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Effect of turmeric on adiponectin, sexual function and sexual hormones in stressed mice


Abstract and Figures

Sexual function is essential for species survival. Melanocortin, progesterone, and estrogen can improve sexual function and they are modulated by adiponectin hormone which can be increased by Turmeric. In various studies shows Turmeric ability that is easily accessible to increase serum adiponectin levels. Therefore, the researchers decided to conduct a study to determine the effect of turmeric on serum adiponectin levels, sexual behavior, and profile of steroid hormones in stressed mice. Thirty female mice, six in each group (1. control group, 2. mice that received stress, 3. stress mice received 100 mg/kg turmeric (extract daily) for 4 weeks, 4. stress mice received turmeric (extract daily) for 4 weeks and also received adiponectin antagonist, and 5. stress groups received adiponectin antagonist), were used in the current study. The mice first underwent blood sampling. Then all mice were subjected to stress testing before the intervention except one group, which considered as a control group. The intervention in this study was done as a 100 mg/kg turmeric extract that was gavaged daily for each mouse. After the intervention, all mice were tested for sexual behavior, and then blood samples were taken to check serum levels of adiponectin, estradiol, progesterone and prolactin. So, the results showed before the intervention there were no significant difference among 5 group in levels of adiponectin (p = 0.145), estradiol (p = 0.148), progesterone (p = 0.166) and prolactin (p = 0.206) but after intervention there were significant difference between 5 group in levels of adiponectin, estradiol and progesterone (p < 0.001). Also there was significant difference among 5 groups in sexual behavior (p < 0.001). Therefore, consumption of turmeric, which increases serum adiponectin in the stressed mice, can improve sexual function and estradiol hormones profiling.
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8Depart ment of Reproductive Health and Mi dwifery, Fa culty of Me dical Scienc es, Tarbiat Modares University, Tehran 14115111, Iran
9Depart ment of Biosta tistics, Fa culty of Me dical Scienc e, Tarbiat Mo dares University, Tehran 14115111, Iran
:Depart ment of Plan t Biology, Ta rbiat Modares University, Tehr an 1411 5111, Iran
;Scho ol of Pharma cy and Ph arma ceut ical Sciences Research Ce nter, Sh ahid Behe shti University of Medi cal Scienc e, Tehran 1411 5111, Iran
<Reprod uctive Biotec hnol ogy Research Cent er, Avicenna Re search Institute, ACECR, Te hran 14115111, Iran
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1. Introduc tion
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E.S. Sahebzad et al. Life Sciences xxx (xxxx) 119575
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2. Materials and methods
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2.4. Measurement of ad iponectin and sexu al ho rmon es
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KIFD@JJ@FE N8J EFK F9J<IM<; N@K?@E K?< ] IJK  D@E F= K?< K<JK K?< D8C<
N8J :8CC<; EFE :FGLC8KFIP 8E; N8 J I<GC8:<; 9P 8EFK?<I D8C< DFLJ<
/?< J<OL8C 9<?8M@FI F= K?< =<D8C< DFLJ< N8J :8 C:LC8K<; 9P ;@M@;@E>
K?< ELD9<I F= K@D<J K?< =<D8C< DFLJ< N8J I<:<GK@M< I<:<GK@M@KP 9P
K?< ELD9<I F= K@D<J K?< DFLEK DLCK@GC@<; 9P  67 $E K?< I<:<GK@M
@KP JK8K < K?< =<D8C< DFLJ< 9<E;J ?<I JG@E< ><K 9<E;@E> GFJKLI< 8E; GLK
?<I C<>J @E 8 JK8E;@E> GFJ@K@FE 2< 8CJF D<8JLI<; K?< I8K< F= J<OL8C
=LE:K@FE N@K? K?< I8K< F= GI<>E8E:P @E D@:< @E <8:? >IFLG
Table 1
FDG8 I@JFE F= 8;@GFE<: K@E <JKI8;@ FC GIF><JK<IFE< 8E ; GIFC8:K@E ?FIDFE< C<M<CJ @E ;@==<I<E K >IFLGJ 9<=FI< K?< @EK<IM<EK@FE
;@GFE<:K@E JKI 8;@F C +IF> <JK<IF E< +IFC 8:K@ E
 \     \    \   \ 
.   \     \    \   \ 
./   \    \    \   \ 
./  \   \    \    \ 
.  \     \    \   \ 
G18 CL<    
E.S. Sahebzad et al. Life Sciences xxx (xxxx) 119575
2.6. Statistical analysis
8K8 N8 J I<GFIK<; 8J D<8EJ \ . ( .K8K@JK@:8C 8E8CPJ@J N8 J G<I
=FID<; LJ@E> "I8G? +8; +I@JD JF=KN8 I< 1<IJ@FE  .?8G@IF2@CB K<JK
N8J LJ<; KF :?<:B K?< ;8K8 EFID8C@KP 8E; G8 I8D<KI@: FI EFE
G8I8D<KI@: JK8 K@JK@:8C K<JKJ N<I< LJ<; =FI K?< 8E8CPJ@J F= EFID8C 8E;
EFEEFID8C ;8K8 ;@JKI@9LK@FE I<JG<:K@M<CP 67 /N FN8P D@O<; 9<
KN<<EN@K?@E 8E8CPJ@J F= M8 I@8E:< )*1 K<JK LJ<; KF :FDG8I<
8;@GFE<:K@E <JKI8;@FC GIF><JK<IFE< 8E; GIFC8:K@E ?FIDFE< C<M<C *E<
N8P )*1 N8 J LJ<; =FI :FDG8I@E> F= J<OL8C 9<?8M@FI /N FJ@;<; G
M8CL<J  N<I< :FEJ@;<I<; JK8K@JK@:8CCP J@>E@=@:8EK ?@ JHL8I< K<JK
LJ<; KF :FDG8I< I8K< F= GI<>E8E:P 9<KN<<E >IFLGJ /8 9C< 
3. Results
3.1. Adiponectin hormone levels
/?< I<JLCKJ J?FN<; K?8K 9<=FI< K?< @EK<IM<EK@FE K?<I< N8J EF J@>E@=
@:8EK ;@==<I<E:< @E 8;@GFE<:K@E ?FIDFE< C<M<C 9<KN<<E K?< ]M< >IFLGJ
G  =K<I @EK<IM<EK@FE :FDG8I<; KF :FEKIFCJ
 \  8;@GFE<:K@E ?FIDFE< C<M<CJ N8J J@>E@=@:8EKCP
G  8E; G  CFN<I @E ./  \  8E; .
 \  D@:< I<JG<:K@M<CP ;@GFE<:K@E ?FIDFE< C<M<C N8 J EFK
:?8E><; @E JKI<JJ  \  8E; ./  \  :FDG8I<;
J@>E@=@:8EKCP G  @E:I<8J<; K?< 8;@GFE<:K@E< C<M<C :FDG8I<; 9<
=FI< KLID<I@: 8;D@E@JKI8K@FE 8E ; LJ@E> KLID<I@: 8EK8>FE@JK J@>E@=@
:8EKCP G  ;<:I<8J<; 8;@GFE<:K@E C<M<C @E ./ >I FLGJ 9LK @E K?@J
JKL;P 8;@GFE<:K@E C<M<CJ N8J EFK :?8E><; @E JKI<JJ 8E; . >IFLGJ
3.2. Estradio l horm one levels
JKI8;@FC C<M<CJ N<I< J@D@C8I 9<KN<<E 8CC >IFLGJ 9<=FI< JK8IK@E> K?<
@EK<IM<EK@FE G  =K<I @EK<IM<EK@FE @E ./  \ 
8E; .  \  >IFLGJ K?< C<M<C F= <JKI8;@FC J@>E@=@:8EKCP
G  N8J CFN<I K?8E :FEKIFC  \  9LK @K N8J EFK
:?8E><; @E JKI<JJ  \  8E; ./  \  >IFLGJ
=K<I FI8C 8;D@E@JKI8K@FE F= KLID<I@: K?< C<M<C F= <JKI8;@FC J@>E@=@:8EKCP
G  @E:I<8J<; @E ./ >IFLG  \  !@> 
3.3. Progesterone ho rmon e levels
/?< C<M<C F= GIF><JK<IFE< N8J J@D@C8I @E 8CC >IFLGJ 9<=FI< @EK<IM<E
K@FE G  J J?FNE @E !@> :FDG8I<; KF K?< :FEKIFCJ K?<
C<M<C F= GIF> <JK<IFE< ?FIDFE< ;<:I<8J<; @E . >IFLGJ /L ID<I@: J@>E@=@
:8EKCP G  @E:I<8J<; K?< GIF><JK<IFE< C<M<C :FDG8I<; KF JKI<JJ
>IFLG +IF><JK<IFE< C<M<C N8 J EFK :?8E><; @E JKI<JJ  \ 
./  \  8E; ./  \  >IFLGJ :FDG8I<; KF
:FEKIFC  \  >IFLGJ !@> 
3.4. Prolac tin horm one le vel
/?< C<M<C F= GIFC8:K@E N8 J EFK J@>E@=@:8 EK ;@==<I<E:< @E 8CC >IFLGJ 9<
=FI< @EK<IM<EK@FE G  =K<I @EK<IM<EK@FE K?< C<M<C F= GIFC8:K@E
N8J EFK J@>E@=@:8EK ;@==<I<E:< 9LK ;<:I<8J<; 8E; 8E8CPJ@J F= F?<EJ ;
J?FN<; 8E <==<:K J@Q< N8J C8I><    8E;  @E ./
. 8E; ./ >IFLGJ I<JG<:K@M<CP !@> 
3.5. Sexu al func tion
.<OL8C 8:K@M@KP J@>E@=@:8EKCP ;<:I<8J<; @E . G  .
G  8E; ./ G  >IFLGJ (<8E \ . ( F= . .
8E; ./ >IFLGJ N8J  \   \  8E;
 \  I<JG<:K@M<CP FDG8I<; KF JKI<JJ >IFLG K?< J<OL8C
9<?8M@FI N8 J J@>E@=@:8EKCP ;<:I<8J<; @E . ./ 8E; . >IFLGJ /?<I<
N8J 8 J@>E@=@:8EK ;@==<I<E:< 9<KN<<E K?< >IFLGJ @E K<IDJ F= K?< ELD9<I
F= GI<>E8 EK D@:< G  /?< ?@>?<JK I8K< F= GI<>E8E:P N8 J @E ./
>IFLG  FDG8I<; KF JKI<JJ >IFLG K?< I8K< F= GI<>E8E:P N8 J
J@>E@=@:8EKCP ;<:I<8J<; @E . ./ 8E; . >IFLGJ
4. Discussion
::FI;@E> KF FLI BEFNC<;>< K?@J JKL;P @J K?< FECP FE< K?8K ?8J =F
:LJ<; FE K?< <==<:K F= KLID<I@: <OKI8:K FE 8;@GFE<:K@E C<M<CJ J<O ?FI
DFE<J 8E; J<OL8C 9<?8M@FI
LE;<I 8EK8>FE@JK @EA<:K@FEJ N8J D@C;<I JF K?@J :FLC; ;L< KF K?< @E:I<8J
@E> @E 8;@GFE<:K@E C<M<CJ 8E; @KJ <==<:K FE J<OL8C 9<?8M@FI @==<I<EK
KPG<J F= JKI<JJ I<;L:< J<OL8C 9<?8M@FI CJF JKI<JJ @E:I<8J<J :8K<:?FC
8D@E<J @E K?< 9I8@E K?8K I<>LC8K< J<OL8C 9<?8M@FI 67
*E K?< FK?<I ?8E;J 8::FI;@E> KF M8I@FLJ JKL;@<J JKI<JJ K<JK@E>
:8LJ<J CFN<I 8; @GFE<:K@E C<M<CJ @E D@:< 67 $E K?< GI<J<EK JKL;P
K?< :FEJLDGK@FE F= KLID<I@: <OKI8:K @E:I<8J<; J<ILD 8;@GFE<:K@E C<M
:I<8J<; J<ILD 8;@GFE<:K@E C<M<CJ DFI< K?8E :FEKIFC >IFLG D@:< N@K?
FLK JKI<JJ J <OG<:K<; K?< JKI<JJ I<;L:<; J<ILD 8;@GFE<:K@E C<M<CJ
;@GFE<:K@E I<;L:<J /)!αC<M<CJ 8E; @E:I<8J<J @EK<IC<LB@E  C<M<CJ
/?<I< @J 8 JKIFE> 8JJF:@8K@FE 9<KN<<E K?< <E;F:I@E< JPJK<D 8E; K?<
E<IM<J ;@GFE<:K@E @J =FLE; @E :<I<9IFJG@E8C ^L@; 8E; 8==<:KJ K?< E<L
IFE8C <O:@K89@C@KP F= JPE8GK@: GC8JK@:@KP 8E; K?< I<C<8J< 8E; I<DF;<C@E>
F= E<LIFEJ 67 CJF @E K?< JKL;P F= $JD8@C@ <K 8C KLID<I@: @J D<E
K@FE<; KF ?8M< <==<:KJ @E I<;L:@E> JKI<JJ C:F?FC@: <OKI8:K F= KLID<I@:
;FG8D@E< J<IFKFE@E 8E; EFI<G@E<G?I@E< $E =8:K 8C:F?FC@: <OKI8: K F=
)#/ 8E; :LI:LD@E :8E GI<M<EK CQ?<@D<IJ 8E; +8IB@EJFEJ ;@J
<8J< 9P I<>LC8K@E> E<LIFKI8E JD@KK<IJ /<@O <@I8 <K 8CJ JKL;P @EM<JK@>8K<J
K?< <==<:KJ F= 8;@GFE<:K@E @E K?< KI<8KD<EK F= +8IB@EJFEJ ;@J<8J< 67
(8EP JKL;@<J ?8M< 8CJF 8;;I<JJ<; K?< @JJL<J F= 8EO@<KP 8E; JKI<JJ @E
F9<J< G<FGC< N@K? D<K89FC@: JPE;IFD< N?@:? :8E 9< 8K KI@9LK<; KF K?<@I
CFN 8;@GFE<:K@E C<M<CJ 67 /?< JKL;P F= .8 C8?J?FF? 8E; :FC
C<8>L<J 8CJF J?FN<; K?< <==<:K F= @E:I<8J@E> 8;@GFE<:K@E =FCCFN@E> K?<
KLID<I@: :FEJLDGK@FE CJF @E 8 JKL;P 9P .8C8?J?FF? <K 8C =8K :<CCJ
Table 2
FDG8 I@JFE F= 8;@GFE<: K@E <JKI8;@ FC GIF><JK<IFE< 8E ; GIFC8:K@E ?FIDFE< C<M<CJ @E ;@==<I<E K >IFLGJ 8=K<I K?< @EK<IM<EK@FE
"IFL G #F ID FE< .<OL 8C 9<?8 M@FI
;@GFE<:K@E JKI8; @FC +I F><JK<IFE< +IFC 8:K@ E
 \   \    \   \    \ 
.   \    \    \    \    \  
./  \   \    \   \    \ 
./  \   \   \    \    \ 
.  \     \    \   \    \  
G18 CL<        
E.S. Sahebzad et al. Life Sciences xxx (xxxx) 119575
Fig. 1. /?< <==<:K F= KLID<I@: FE 8;@GFE<: K@E C<M<C -<JLCKJ 8I<
D<8E \ . ( ) >IFLG G  8E ; G  :FDG8I<; KF
:FEKIFC  G  :FD G8I< ; KF JKI<JJ >IFLG 8E ; G  8E;
G  :FD G8I<; KF 9< =FI< @EK<IM<EK@FE
Fig. 2. /?< <==<:K F= KLID<I@: FE <JKI8;@FC C<M<C -<JLCKJ 8I< D< 8E \ . (
) >IFLG G  :FDG8I<; KF :FEKIFC 8E; G   :FD
G8I<; KF 9< =FI< @EK<IM<EK@FE
Fig. 3. /?< <==<:K F= KLID <I@: FE GI F><JK<IFE< C<M<C -<JL CKJ 8I<
D<8E \ . ( ) >IFLG G  :FDG8I<; KF :FE KIFC 8E;
G   :FDG8I<; KF JKI< JJ >IFLG
N<I< G@:B<; LG =F CCFN@E> M@J:<I8C =8 K JLI><IP 8E; N<I< KI<8K<; N@K?
:LI:LD@E J 8 I<JLCK K?< J<:I<K@FE F= @EK<IC<LB@E 8E; 8;@GFE<:K@E
=IFD K?<J< :<CCJ @E:I<8J<; 67 /LID<I@: <OKI8:K GIFK<:KJ 8>8@EJK FO
@;8K@M< JKI<JJ 9P :I<8K@E> 8 98C8E:< 9<KN<<E 8EK@FO@;8EK ;<=<EJ< 8E;
K?< -*. I<8:K@M< FO P><E JG<:@<J JPJK<D 8E; N< :8E :FEJ@;<I K?< 98C
Fig. 4. /?< <==<:K F= KLID <I@: FE GIFC8:K@E C<M<C -<JLCKJ 8I< D<8E \ . (
) >IFLG
8E:< GIF:<JJ 8J 8 N8P F= @DG8:K FE K?< <E;F><EFLJ JPJK<D 67 !@>
::FI;@E> KF M8I@FLJ JKL;@<J K?<I< @J 8 C@EB 9<KN<<E 8;@GFE<:K@E
C<M<CJ 8E; FM8I@8E JK<IF@;F><E<J@J @E JKI<JJ<; D@:< 67 (8EP 8IK@:C<J
?8M< JL>><JK<; 8 C@EB 9<KN<<E @E:I<8J< @E K?< C<M<C F= JK<IF@; ?FIDFE<J
8E; @DGIFM<; J<OL8C 9<?8M@FI $E =8:K K?< 8EK@FO@;8EK 8E; 8EK@
@E^8DD8KF IP 8:K@M @KP F= :LI:LD@E @DGIFM<J J<OL8C 8: K@M@KP 67 $E FLI
F= /8 BFI <K 8C ::FI;@E> KF K?< ]E;@E>J F= K?<@I JKL;P K?< 8CB8CF@;J
8E; ^8MFEF@;J @E K?< 8C:F?FC@: <OKI8:K F= KLID<I@: @E:I<8J< K?< C<M<C F=
<JKI8;@FC N?@:? @E KLIE @E:I<8J< K?< J@Q< F= K?< LK<ILJ 8E; FM 8I@<J 67
/LID<I@: <OKI8:K @E I8K D@:< ?8J 8 GIF8GFGKFK@: GIFE<IFK@: 8E; 8E
K@GIFC@=<I8K@M< <==<:K 8E; GIFK<:KJ FF>FE@8 :<CCJ 8>8@EJK JKI<JJ /?<
D<:?8E@JD 9P N?@:? KLID<I@: 8==<:KJ K?< I<GIF;L:K@M< JPJK<D @J JK@CC
LEBEFNE 9LK @K :8E 9< ;<G<E;<EK FE K?< >IFN K? F= =FCC@:LC8I 9CFF; M<J
C<GK@E 8E; 8;@GFE<:K@E $E K?< GI<J<EK JKL;P K?< LJ< F= KLID<I@: <OKI8:K
@E 8EK8>FE@JK @EA<:K@FE >IFLGJ ;@; EFK @E:I<8J< <JKI8;@FC 8E; GIF><J
K<IFE< C<M<CJ ::FI;@E> KF K?<J< ]E;@E>J @K :8E 9< :C8@D<; K?8K
KLID<I@: <OKI8:K ?8J 8E @E:I<8J@E> <==<:K FE <JKI8;@FC 8E; GIF><JK<IFE<
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8;@GFE<:K@E FE @E:I<8J@E> <JKI8;@FC 8E; GIF><JK<IFE< 8E; 8::FI;@E> KF
Fig. 5. /? < <==<:K F= KLID<I@: FE J<OL8C 9< ?8M@FI -<JLCKJ 8I< D<8E \ . (
) >IFLG G   8E; G  :FDG8I<; KF :FEKIFC
+   8E;  G   :FDG8I<; KF JKI<JJ >IFLG
E.S. Sahebzad et al. Life Sciences xxx (xxxx) 119575
Fig. 6. /? < <==<:K F= KLID <I@: FE GI <>E8E:P I8K< @E <8:? >IFL G
K?<@I ]E;@E>J 8;@GFE<:K@E @E:I<8J<J K?< JK<IF@;F><E<J@J F= FM8I@8E
>I8ELCFJ8 :<CCJ /?<I< @J <M@;<E:< F= <O@JK@E> F= 8;@GFE<:K@E I<:<GKFIJ
;@GFI 8E; $+*- @E K?< ?PGFK?8C8DLJ N?@:? :8E GC8P 8 IFC< @E
K?< D8KLI8K@FE 8E; I<GIF;L:K@M< DLK8 K@FE @E K?< 8;@GFE<:K@E ><E<
I<;L:<J ")-# 8E; ;@JILGKJ K?< D@:<J <JKIFLJ :P:C< /?< GI<J<E:< F=
8;@GFE<:K@E @E K?< :<I<9IFJG@E8C ^L@; D8P @E;@:8K< @KJ IFC< @E K?< G@KL
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8;@GFE<:K@E @E:I<8J<J K?< J<:I<K@FE F= <JKI8;@FC 8E; GIF><JK<IFE< =IFD
>I8ELCFJ8 :<CCJ $E 8;;@K@FE K?< I<DFM8C F= K?< 8;@GFE<:K@E ><E< @E
D@:< :8LJ<J GIF9C<DJ N@K? JK<IF@;F><E<J@J 8E; @DG8@IJ K?< =<IK@C@KP 8E;
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N?@:? @E:I<8J<J K?< J<:I<K@FE F= GIF><JK<IFE< =IFD =FCC@:C< :<CCJ ! 8E;
! 9P =FCC@:C<J FEK8:K N@K? @JF=C8MFEF@;J @E:I<8J<J 8;@GFE<:K@E C<M<CJ
67 !@> 
5. Conclusion
::FI;@E> KF K?< ;8K8 F9K8@E<; @E K?@J JKL;P @K :8E 9< <OG<:K<; K?<
:FEJLDGK@FE F= KLID<I@: N?@:? @E:I<8J< J<ILD 8;@GFE<:K@E @E K?<
?FIDFE<J 9P @E:I<8J@E> K?< J<ILD 8;@GFE<:K@E C<M<CJ
/8I9@8K (F;8I<J 0E@M<IJ@KP JLGGFIK<; K?< GIFA<:K 8J 8 +? K?<J@J @E
K<ID F= ;<J@>E F= JKL;P :FCC<:K@FE 8E8CPJ@J @EK<IGI<K8K@FE F= ;8K8 8E;
NI@K@E> K?< D8ELJ:I@GK 8GGIFM8C :F;< 
Ethics approval
/?< <K?@:J :FDD@KK<< F= JKL;P /8 I9@8K (F ;8I<J 0E@M<IJ@KP N@K?
<K?@:J :F;< F= $-(*- .- 
Availability of data and material
Decl aration of competing intere st
/?< 8LK?FIJ ;<:C8I< K?8K K?<I< @J EF :FE^@:K F= @EK<I<JK 9<KN<<E 8L
/?< JKL;P N8J G8IK F= +? 8K <G8IKD<EK F= (@;N@=<IP 8E; -<GIF
;L:K@M< #<8CK? !8:LCKP F= (< ;@:8C .:@<E:< /8I9@8K (F;8I<J 0E@M<IJ@KP
/?< 8LK?FIJ 8GGI<:@8K< K?< :FCC89FI8K@FE F= K?< -<J<8I:? $EJK@KLK< F=
E;F:I@E< .:@<E:< 8E; (<K8 9FC@JD .?8?@; <?J?K@ 8E; @KJ D8E8><I I
(<?;@ #<;8P8K @ 8E; !8I@98 8B?K@P8IQ8;<
Referenc es
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9<?8M@ FI @E K?< ?L D8 E =< D8 C< % "<E +J P:?FC    FF B -<M@<N
67 + 9<;@ ( =I8Q<? ) %8 M8;@ =8I  .8 B@ /?< I<C8 K@FE 9<KN<<E JK I<JJ 8E;
J<OL 8C =LE:K@ FE 8E; J8 K@J= 8:K@ FE @E I<GIF;L:K@M< 8>< NF D<E @E $I8E 8 :IFJJ
J<:K@F E8C JK L;P % .< O (8 I@K8 C /?<I   
67 - C FB . 8J " >8I N8 C ' .8 CN8?8E - .I @M8J K8 M8 -<C8K@ FEJ?@G F=
J<M<I@ KP F= ;<GI<JJ@ FE 8E O@<KP 8E ; JKI<JJ N@ K? J<M<I@ KP F= ]9I FD P8C> @8 C@E
OG -?<LD8 KFC $E:C .LGGC<D< EKJ   . 
67 (  .K<G?<EJ " 28 E; .K I<JJ 8E ; K?< #+ 8O@ IF C< F= >CL:F:FI K@:F@; J @E
8C:F?FC ;<G<E;<E:< C:F?F C -<J L II -<M 
67 "+ ?IF LJFJ % /FIGP + 2 "FC; $EK<I8 :K@FEJ 9<KN<<E K?<
?PGF K?8C 8D @:G@ KL@K8I P 8;I< E8C 8O @J 8E ; K?< =<D8 C< I<GIF; L:K@M< JP JK <D
:C@E@:8C @D GC@: 8K@F EJ EE $EK<IE (< ;   
67 . ( 18 E E;<IJ ' IFK KF % !8 II<CC ( 4L C< J JF:@ 8K@F EJ 8D FE>
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JK<I F@; ?FID FE <J @E ?<8C K?P GI <D<EFG8L J8 C NF D<E % .< O (< ; 
67 . CY?<I ( 5@FK FGFLCF L %2 LCC<E .% (FJ:?F J ' 0E>JLE 8E
&FBB FKFL (8I8 KFJ!C @<I . (8EKQFIFJ -<JG FEJ@ M<E<JJ KF G<I@ G?<I 8CCP
8;D@ E@ JK <I<; D<C8 EF :FIK @EJ @E C<8E 8E; F9<J < D@:< @89 <K<J  
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(<K8 9   
67  ?89IFCC < ' /FJ:8  -8 DS + '<:FDK <  -FPTI< % LGFEK
;@G FE<:K@E @E :I<8 J<J @E JLC@ EC@ B< >I FN K? =8:KFI $@E;L:<; GI F><J K<IF E< 8E;
<JKI 8;@F C J<:I<K@F E @E ?LD8 E >I8E LCFJ 8 :<CCJ !<IK@C .K<I @C  
67 . &@D & (8IH L8I; . .K<G?<EJ 'FL;<E % CCJ NFIK ? & (FC<P
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E.S. Sahebzad et al. Life Sciences xxx (xxxx) 119575
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... The combination of mefenamic acid and turmeric can alleviate pain in primary dysmenorrhea (PDM) in women [72]. Turmeric can increase estradiol hormone profiling and sexual function [73]. Its residue, which is a solid waste from the curcuminoid industry, can be applied as the major material for making ceramic foam [74]. ...
Background: Turmeric (Curcuma longa L.), belonging to the Zingiberaceae family, is a perennial rhizomatous plant of tropical and subtropical regions. The three major chemical components responsible for the biological activities of turmeric are curcumin, demethoxycurcumin, and bisdemethoxycurcumin. Method: The literature search included review articles, analytical studies, randomized control experiments, and observations, which have been gathered from various sources, such as Scopus, Google Scholar, PubMed, and ScienceDirect. A review of the literature was carried out using the keywords: turmeric, traditional Chinese medicine, traditional Iranian medicine, traditional Indian medicine, curcumin, curcuminoids, pharmaceutical benefits, turmerone, demethoxycurcumin, and bisdemethoxycurcumin. The main components of the rhizome of the leaf are α-turmerone, β-turmerone, and arturmerone. Result: The notable health benefits of turmeric are antioxidant activity, gastrointestinal effects, anti-cancer effects, cardiovascular and antidiabetic effects, antimicrobial activity, photoprotector activity, hepatoprotective and renoprotective effects, and appropriate for the treatment of Alzheimer's disease and inflammatory and edematic disorders. Discussion: Curcuminoids are phenolic compounds usually used as pigment spices with many health benefits, such as antiviral, antitumour, anti-HIV, anti-inflammatory, antiparasitic, anticancer, and antifungal effects. Curcumin, bisdemethoxycurcumin, and demethoxycurcumin are the major active and stable bioactive constituents of curcuminoids. Curcumin, which is a hydroponic polyphenol, and the main coloring agent in the rhizomes of turmeric, has anti-inflammatory, antioxidant, anti-cancer, and anticarcinogenic activities, as well as beneficial effects for infectious diseases and Alzheimer's disease. Bisdemethoxycurcumin possesses antioxidant, anti-cancer, and anti-metastasis activities. Demethoxycurcumin, which is another major component, has anti-inflammatory, antiproliferative, and anti-cancer activities and is the appropriate candidate for the treatment of Alzheimer's disease. Conclusion: The goal of this review is to highlight the health benefits of turmeric in both traditional and modern pharmaceutical sciences by considering the important roles of curcuminoids and other major chemical constituents of turmeric. .
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RationaleMany depressed women continue antidepressant treatment during pregnancy. Selective serotonin reuptake inhibitor (SSRI) treatment during pregnancy increases the risk for abnormal social development of the child, including increased aggressive or defiant behavior, with unknown effects on sexual behavior.Objectives Our aim was to investigate the effects of perinatal SSRI treatment and maternal depression, both separately and combined, on aggressive and sexual behavior in male rat offspring.Methods Heterozygous serotonin transporter (SERT± ) knockout dams exposed to early life stress (ELSD) were used as an animal model of maternal depression. Early life stress consisted of separating litters from their mother for 6 h a day on postnatal day (PND)2–15, resulting in a depressive-like phenotype in adulthood. Depressive-like dams were treated with fluoxetine (FLX, 10 mg/kg) or vehicle throughout pregnancy and lactation (gestational day 1 until PND 21). Male offspring were tested for aggressive and sexual behavior in adulthood. As lifelong reductions in SERT expression are known to alter behavioral outcome, offspring with normal (SERT+/+) and reduced (SERT± ) SERT expression were assessed.ResultsPerinatal FLX treatment reduced offensive behavior and the number of animals attacking and increased the latency to attack, especially in SERT+/+ offspring. Perinatal FLX treatment reduced the mounting frequency in SERT+/+ offspring. ELSD increased offensive behavior, without affecting sexual behavior in SERT± offspring.Conclusions Overall, our research demonstrates that perinatal FLX treatment and ELSD have opposite effects on aggressive behavior, with little impact on sexual behavior of male offspring.
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Abstract Background The rate of cesarean section is increasing worldwide. Adiponectin is a hormone related to anti-inflammatory and anti-atherogenic effects; and it′s concentrations may change in response to inflammatory situations including surgical intervention. The aim of the current study was to investigate serum adiponectin levels in maternal and umbilical cord blood according to different modes of delivery and their relationship with anthropometric measurements and fetal sex. Methods The study population initially comprised 90 healthy pregnant women referred to the teaching hospital. Eventually, 40 participants in the vaginal delivery group and 35 subjects in the cesarean delivery group were recruited in to the study. Umbilical cord blood and maternal serum samples were analyzed according to the standard protocol from the manufacturer. The collected data were analyzed using SPSS-16 software. P-value
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Adiponectin is the most abundant plasma adipokine. It mainly derives from white adipose tissue and plays a key role in the control of energy metabolism thanks to its insulin-sensitising, anti-inflammatory, and antiatherogenic properties. In vitro and in vivo evidence shows that adiponectin could also be one of the hormones controlling the interaction between energy balance and fertility in several species, including humans. Indeed, its two receptors—AdipoR1 and AdipoR2—are expressed in hypothalamic–pituitary–gonadal axis and their activation regulates Kiss, GnRH and gonadotropin expression and/or secretion. In male gonads, adiponectin modulates several functions of both somatic and germ cells, such as steroidogenesis, proliferation, apoptosis, and oxidative stress. In females, it controls steroidogenesis of ovarian granulosa and theca cells, oocyte maturation, and embryo development. Adiponectin receptors were also found in placental and endometrial cells, suggesting that this adipokine might play a crucial role in embryo implantation, trophoblast invasion and foetal growth. The aim of this review is to characterise adiponectin expression and its mechanism of action in male and female reproductive tract. Further, since features of metabolic syndrome are associated with some reproductive diseases, such as polycystic ovary syndrome, gestational diabetes mellitus, preeclampsia, endometriosis, foetal growth restriction and ovarian and endometrial cancers, evidence regarding the emerging role of adiponectin in these disorders is also discussed.
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Emerging evidence from the preclinical and human research suggests sex differences in response to different types of stress exposure, and that developmental timing, reproductive status, and biological sex are important factors influencing the degree of HPA activation/function. Here we review data regarding: i) sex differences inbehavioral and neural responses to uncontrollable and controllable stressors; ii) distinct trajectories of behavioral development and HPA-axis function in male and female rats following adolescent stress exposure; iii) normative changes in behavior and dopamine function in early postpartum rats; iv) aberrant HPA-axis function and its link to abnormal behaviors in two independent, preclinical mouse models of postpartum depression; and,v) data indicating that gender, in addition to sex, is an important determinant of stress reactivity in humans.Based on these findings, we conclude it will be important for future studies to investigate the short and long-term effects of a wide variety of stressors, how these effects may differ according to developmental timing and in relation to gonadal function, the relationship between aberrant HPA-axis activity during the postpartum and mood disorders, and influences of both sex and gender on stress reactivity in humans.
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The present study investigated whether dietary turmeric (Curcuma longa L.) can improve rabbit reproduction, ovarian function, growth, or viability. Female New Zealand White rabbits were either fed a standard diet (n=15) or a diet enriched with 5 g (group E1) or 20 g (group E2) turmeric powder per 100 kg feed mixture (n=16 or 15, respectively). After 295 days, weight gain, conception and kindling rates, pup and mother viability, ovarian macro- and micro-morphometric indices, release of leptin in response to the addition LH, and the release of progesterone, testosterone and leptin by isolated ovarian fragments were analyzed. Dietary turmeric failed to affect ovarian length and weight but did increase the number of primary follicles (E2: 32.5% greater than control group), as well as the diameter of primary (E1: +19.4%, E2: +21.1%), secondary (E2: +41.4%), and tertiary (E1: +97.1%, E2: +205.1%) follicles. Turmeric also increased the number of liveborn (E1: +21.0%) and weaned (E1: +25.0%) pups and decreased the number of stillborn pups (E2: −87.5%) but did not affect weight gain, conception, or kindling rate. Furthermore, dietary turmeric decreased doe mortality during the first reproductive cycle (13.3% in control; 0% in E1; and 6.7% in E2) but not during the second cycle. In vitro, the ovaries of the turmeric-treated rabbits released more progesterone (E1: +85.7%, E2: +90.0%) and less testosterone (E2: −87.0%) and leptin (E2: −29.0%) than the ovaries of control rabbits. Moreover, LH decreased the leptin output of control rabbits but increased that of experimental rabbits. Therefore, it is likely that dietary turmeric improves pup viability and that it could promote rabbit fecundity by either (1) promoting the production of primary ovarian follicles or (2) stimulating the growth of follicles at all stages of folliculogenesis.
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Adiponectin, the most abundant plasma adipokine, plays an important role in the regulation of glucose and lipid metabolism. Adiponectin also possesses insulin-sensitizing, anti-inflammatory, angiogenic, and vasodilatory properties which may influence central nervous system (CNS) disorders. Although initially not thought to cross the blood-brain barrier, adiponectin enters the brain through peripheral circulation. In the brain, adiponectin signaling through its receptors, AdipoR1 and AdipoR2, directly influences important brain functions such as energy homeostasis, hippocampal neurogenesis, and synaptic plasticity. Overall, based on its central and peripheral actions, recent evidence indicates that adiponectin has neuroprotective, antiatherogenic, and antidepressant effects. However, these findings are not without controversy as human observational studies report differing correlations between plasma adiponectin levels and incidence of CNS disorders. Despite these controversies, adiponectin is gaining attention as a potential therapeutic target for diverse CNS disorders, such as stroke, Alzheimer’s disease, anxiety, and depression. Evidence regarding the emerging role for adiponectin in these disorders is discussed in the current review.
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17β-Estradiol (E2) regulates the expression of female sexual behavior by acting through estrogen receptor (ER) α and β. Previously, we have shown that ERβ knockout female mice maintain high level of lordosis expression on the day after behavioral estrus when wild-type mice show a clear decline of the behavior, suggesting ERβ may be involved in inhibitory regulation of lordosis. However, it is not identified yet in which brain region(s) ERβ may mediate an inhibitory action of E2. In this study, we have focused on the dorsal raphe nucleus (DRN) that expresses ERβ in higher density than ERα. We site specifically knocked down ERβ in the DRN in ovariectomized mice with virally mediated RNA interference method. All mice were tested weekly for a total of 3 weeks for their lordosis expression against a stud male in two consecutive days: day 1 with the hormonal condition mimicking the day of behavioral estrus, and day 2 under the hormonal condition mimicking the day after behavioral estrus. We found that the level of lordosis expression in ERβ knockdown (βERKD) mice was not different from that of control mice on day 1. However, βERKD mice continuously showed elevated levels of lordosis behavior on day 2 tests, whereas control mice showed a clear decline of the behavior on day 2. These results suggest that the expression of ERβ in the DRN may be involved in the inhibitory regulation of sexual behavior on the day after behavioral estrus in cycling female mice.
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Adaptive responses to stressful stimuli involving behavioral, emotional and metabolic changes are orchestrated by the nervous and endocrine systems. Adipose tissue has been recognized as a highly active metabolic and endocrine organ, secreting adipokines that operate as hormones to mediate the crosstalk with other organs including the brain. The role of adipose tissue in sensing and responding to emotional stress and in behavioral regulation, however, remains largely unknown. The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) is a key transcriptional factor controlling adipokine gene expression. Here we show that chronic social defeat stress decreases messenger RNA and protein levels of PPARγ in adipose tissue of susceptible but not resilient mice, which was correlated with social avoidance behavior. A corresponding reduction in adipose adiponectin production was observed in susceptible mice. Rosiglitazone, a blood–brain barrier-impermeant PPARγ-selective agonist, elicited antidepressant- and anxiolytic-like behavioral effects in wild-type mice, with a concurrent increase in plasma adiponectin levels. These effects of rosiglitazone were absent in mice lacking adiponectin but having normal PPARγ expression in adipose tissue and brain. Moreover, pretreatment with the PPARγ-selective antagonist GW9662 blocked rosiglitazone-induced adiponectin expression and antidepressant/anxiolytic-like effects. Together, these results suggest that the behavioral responses to rosiglitazone are mediated through PPARγ-dependent induction of adiponectin. Our findings support an important role for the adipose PPARγ-adiponectin axis in susceptibility to stress and negative emotion-related behaviors. Selectively targeting PPARγ in adipose tissue may offer novel strategies for combating depression and anxiety.
In this study, the phenolic profiles and bioactivities (antioxidant and antiproliferative activities) of turmeric extracts obtained by ultrasound-assisted extraction (UAE) and conventional solvent extraction (CSE) were compared. The results showed that UAE and CSE had significant effects (p < 0.05) on phenolic composition, antioxidant activities, and antiproliferative effects. Compared with CSE, UAE can significantly (p < 0.05) increase extraction efficiency of phenolic compounds. Turmeric extracts obtained by UAE exhibited stronger antiproliferative effects against a panel of cancer cell lines (MCF7, MDA-MB-231, HCT116, HT29, HepG2, HeLa) than that obtained by CSE. In addition, the turmeric extracts can reduce the generation of reactive oxygen species (ROS), inhibit cell migration, induce cell morphological changes and nuclear condensation, and arrest cell cycle at S and G2/M phases. The present findings suggested that ultrasonication can be applied successfully for the extraction of bioactive constituents from turmeric with enhanced biological activities, and the turmeric extracts have antiproliferative effects which may be mediated through ROS modulation and cell cycle arrest. Overall, turmeric extracts can be considered as a potential source of bioactive compounds for the treatment of cancer-related diseases.
Adiponectin, which is secreted specifically by adipose tissue, has been shown to have anti-atherogenic and anti-inflammatory effects and to improve insulin resistance (IR). The aim of this study was to determine the correlations among adiponectin, IR and atherosclerosis in non-diabetic hypertensive patients and healthy volunteers. In this case control study, we collected complete demographic data from and measured several laboratory parameters in all enrolled subjects. The homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated as an insulin sensitivity index. The atherogenic index of plasma (AIP), which is calculated as log (triglyceride (TG)/high-density lipoprotein cholesterol (HDL-C)), was a significant predictor of atherosclerosis and was a better predictor of atherosclerosis than low-density lipoprotein cholesterol (LDL-C). Plasma adiponectin, interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1) and matrix metalloprotein-9 (MMP-9) concentrations were determined using enzyme-linked immunosorbent assay (ELISA). All data were analyzed using Statistical Product and Service Solutions for Windows (SPSS) 13.0 software. A total of 309 participants were enrolled in the study. Hypertensive patients with IR (n = 93) displayed significantly higher HOMA-IR values and AIPs and lower adiponectin levels than hypertensive patients without IR (n = 121) and healthy adults (n = 95) (P < 0.05). Furthermore, circulating IL-6, MCP-1 and MMP-9 concentrations differed significantly between hypertensive patients and healthy adults (P < 0.05). Additionally, adiponectin levels were found to be inversely correlated with IL-6, MCP-1, and MMP-9 levels; HOMA-IR values; and AIPs in the clinical study. HOMA-IR values and adiponectin and creatinine (Cr) concentrations remained independently associated with AIPs in all participants after adjustment for confounders via multivariate linear regression. Low adiponectin levels are positively correlated with decreased insulin sensitivity, increased pro-inflammatory cytokine production and worsening atherosclerosis in hypertensive patients and healthy adults.