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ABSTRACT: AIM: Cisplatin chemotherapy is associated with neurotoxicity, and oxidative stress might play an important role in the pathogenesis. Mirtazapine may be a preventative agent via its less-known antioxidant properties. The aim of this study was to examine the potential chemoprotective effects of mirtazapine against cisplatin-induced oxidative stress and DNA damage. METHODS: Twenty-four rats were divided equally into four groups: control; cisplatin (10 mg/kg i.p.); cisplatin plus mirtazapine (10-30 mg/kg, respectively i.p and p.o.); and mirtazapine (30 mg/kg p.o.). The rats were killed at the end of the 14th day of treatment. Brain tissue was examined with regard to antioxidant/oxidant biochemical parameters. RESULTS: Although glutathione (tGSH) and nitric oxide (NO) end product mean scores were found to be statistically higher in the control group when compared with the cisplatin group (72.44% and 61.99% percentage change [PC], respectively), malondialdehyde (MDA), myeloperoxidase (MPO), and 8-hydroxyguanine (8-OH-GUA) mean scores were statistically lower in the control group in comparison with the cisplatin group (-55.48%, -67.99%, and -48.81% PC, respectively; P < 0.01). Finally, tGSH and NO end product levels were restored to normal (85.90% and 55.30% PC, respectively), and MDA, MPO, and 8-OH-GUA were significantly reduced by treatment with mirtazapine (-60.50%, -78.59%, and -38.10% PC, respectively; P < 0.01). CONCLUSION: Mirtazapine has chemoprotective effects against cisplatin-induced oxidative stress and DNA damage in the rat brain, which may be attributed to its antioxidant capabilities. It would be useful to investigate whether cisplatin at the desired doses can be given concurrently with mirtazapine.
Psychiatry and Clinical Neurosciences 12/2012; · 2.13 Impact Factor
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ABSTRACT: Reperfusion has always been "the emergency intervention" to ischemic tissue. For a given period of time, tissue injury due to ischemia and reperfusion is more serious than injury due to ischemia only. Groups were as: Group 1: 25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 2: 10 mg/kg yohimbine +25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 3: Ischemia/reperfusion (control) group. Group 4: Healthy rats. Rat ovaries were exposed to a 3-hour ischemia and then reperfusion ensured for 2 hours. After ischemia/reperfusion, total glutathione, malondialdehyde, 8-hydroxyguanine levels and histopathological investigation were studied. The highest total glutathione and the lowest malondialdehyde and DNA damage levels were determined in dexmedetomidine group when compared to control group. The difference between yohimbine + dexmedetomidine and the control group was insignificant. Dexmedetomidine protects the ovarian tissue of the rat from I/R injury. It is hypothesized that this protective effect of dexmedetomidine is mediated by the α-2 adrenergic receptors. Dexmedetomidine could be useful for attenuation of tissue damage after I/R and prevention of I/R-related complications.
Gynecological Endocrinology 12/2012; · 1.58 Impact Factor
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ABSTRACT: Background: Oxidative liver injury occurring with methotrexate restricts its use in the desired dose. Therefore, whether or not thiamine and thiamine pyrophosphate, whose antioxidant activity is known, have protective effects on oxidative liver injury generated with methotrexate was comparatively researched in rats using biochemical and histopathological approaches. Material/Methods: Thiamine pyrophosphate+methotrexate, thiamine+methotrexate, and methotrexate were injected intraperitoneally in rats for 7 days. After this period, all animals' livers were excised, killing them with high-dose anesthesia, and histopathologic and biochemical investigations were made. Result: Biochemical results demonstrated a significant elevation in level of oxidant parameters such as MDA and MPO, and a reduction in antioxidant parameters such as GSH and SOD in the liver tissue of the methotrexate group. Also, the quantity of 8-OHdG/dG, a DNA injury product, was higher in the methotrexate group with high oxidant levels and low antioxidant levels, and the quantity of 8-OHdG/dG was in the thiamine pyrophosphate group with low oxidant levels and high antioxidant levels. In the thiamine and control groups, the 8-OHdG/dG rate was 1.48±0.35 pmol/L (P>0.05) and 0.55±0.1 pmol/L (P<0.0001). Thiamine pyrophosphate significantly decreased blood AST, ALT and LDH, but methotrexate and thiamine did not decrease the blood levels of AST, ALT and LDH. Histopathologically, although centrilobular necrosis, apoptotic bodies and inflammation were monitored in the methotrexate group, the findings in the thiamine pyrophosphate group were almost the same as in the control group. Conclusions: Thiamine pyrophosphate was found to be effective in methotrexate hepatotoxicity, but thiamine was ineffective.
Medical science monitor: international medical journal of experimental and clinical research 12/2012; 18(12):BR475-481. · 1.70 Impact Factor
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ABSTRACT: Cisplatin is a platinum derivative frequently used in the chemotherapy of different solid tumors. This biochemical and histologic study investigated a possible protective effect of mirtazapine with regard to cisplatin-induced nephrotoxicity in the rat.
The animals were divided into 4 groups: 15 mg/kg mirtazapine + 10 mg/kg cisplatin, 30 mg/kg mirtazapine + 10 mg/kg cisplatin, only 10 mg/kg cisplatin and negative control (healthy) group. During 14 days, the treatment and treated control group took drugs, while the healthy animals were given distilled water on the same schedule. All animals were sacrificed by high-dose anesthesia at the end of the 14 days of treatment; their kidneys were removed and subjected to histologic and biochemical study.
In both of the doses we used, mirtazapine decreased the levels of malondialdehyde, creatinine, blood urea nitrogen and myeloperoxidase activity when compared to cisplatin group. On the other hand, it increased total glutathione level in all doses. Slight histopathological findings were determined in mirtazapine groups when compared to cisplatin control group.
In the light of our results and literature knowledge, we can conclude that the protective effect of mirtazapine in cisplatin toxicity originates from its own antioxidant activity.
Pharmacological reports: PR 05/2012; 64(3):594-602. · 2.44 Impact Factor
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ABSTRACT: In this study, the effects of nimesulide on the antiinflammatory and ulcerative action of some nonsteroidal antiinflammatory
drugs (NSAIDs; (diclofenac sodium, ibuprofen, meloxicam) were investigated in rats, and it was determined whether nimesulide
interacts with these drugs in vivo and in vitro. Results showed that while diclofenac sodium, ibuprofen, and meloxicam reduced carrageenan-induced paw edema in rats by 66%,
39.6%, and 58%, respectively, when used alone, they reduced carrageenan-induced paw edema by 69.8%, 56.6%, and 66%, respectively,
when combined with nimesulide. Diclofenac (25 mg kg-1) and meloxicam (7.5 mg kg-1) produced 9.3 and 19.6 mm2 ulcer areas in stomachs of rats, respectively, when used alone, but when combined with nimesulide diclofenac and meloxicam
did not cause any injury in rat stomachs. While ranitidine at 100 mg kg-1 dose prevented diclofenac-induced ulcer formation, it reduced meloxicam-induced ulcer formation significantly. We conclude
that nimesulide does not interact with these drugs in terms of antiinflammatory action and antagonizes their side effects
on gastric tissue without reacting chemically.
Medicinal Chemistry Research 04/2012; 16(2):78-87. · 1.27 Impact Factor
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ABSTRACT: In this study, effects of Lacidipine (LAC), Ramipril (RAM) and Valsartan (VAL) on DNA damage and oxidative stress occurred
in acute and chronic periods after isoproterenol (ISO)-induced myocardial infarct (MI) were investigated in rats. LAC, RAM
and VAL had been administered by oral gavage at 3, 3 and 30mg/kg doses, respectively, in acute and chronic periods following
MI. In acute MI model, LAC, RAM and VAL had been administered once per day to rat groups during 30days. On days 29 and 30,
the rats of the acute MI control and drug treatment groups were administered 180mg/kg ISO, subcutaneously at an interval
of 24h. In chronic MI model, LAC, RAM and VAL had been administered to rat groups during 30days, and on the 1st and 2nd
days, the rats of the chronic MI control and drug treatment groups were administered ISO, by the same way. After this period,
routine biochemistry indicators of MI, alanin aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase
(LDH), creatine kinase (CK), creatine kinase-isoenzymes (CK-MB), troponin I (TnI) and nitric oxide (NO), oxidative stress
indicator, has been measured in the serums obtained from rat’s blood. Also, 7,8-Dihydro-8-oxo-guanine (8-OHGua), which is
an indicator of DNA damage level, has been determined in whole blood. After MI diagnosis, the relationships among the 8-OHGua,
NO and clinic MI indicators have been determined. Results have been evaluated by comparing with that of control group. In
control groups, the clinic MI indicators have been found to be statistically higher than the drug groups. In parallel to this
increase in MI indicators, there have been determined a significant decrease in NO levels and an increase in 8-OHGua level.
There was no significant difference in the rat groups which received drugs without MI induction. We have observed that the
level of 8-OHGua which increased after MI in both acute and chronic periods decreased by LAC, RAM and VAL when compared to
acute and chronic MI control groups. In conclusion, it has been determined that oxidative stress has been increased after
ISO induced MI model and this stress reduces NO and even damages DNA. LAC, RAM and VAL may decrease the severity of MI and
prevent DNA damage by reducing oxidative stress.
Molecular and Cellular Biochemistry 04/2012; 328(1):109-117. · 2.06 Impact Factor
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ABSTRACT: The ability of amiodarone to prevent pathological changes and oxidative stress after isoproterenol (ISO)-induced myocardial The ability of amiodarone to prevent pathological changes and oxidative stress after isoproterenol (ISO)-induced myocardial
injury was investigated in rats. A better understanding of the processes involved in the pathophysiology of myocardial infarction injury was investigated in rats. A better understanding of the processes involved in the pathophysiology of myocardial infarction
has led to the search for drugs that can limit the extent of myocardial injury. Amiodarone was administered to groups of rats has led to the search for drugs that can limit the extent of myocardial injury. Amiodarone was administered to groups of rats
groups once per day for 30days. On days 29 and 30, the rats of the ISO control and drug treatment groups were administered groups once per day for 30days. On days 29 and 30, the rats of the ISO control and drug treatment groups were administered
180mg/kg ISO subcutaneously at an interval of 24h for two consecutive days. In the control groups, clinical indicators, 180mg/kg ISO subcutaneously at an interval of 24h for two consecutive days. In the control groups, clinical indicators,
such as creatine kinase-isoenzymes and troponin-I, were found to be statistically higher than in the drug groups. Parallel such as creatine kinase-isoenzymes and troponin-I, were found to be statistically higher than in the drug groups. Parallel
to this increase in indicators, a significant decrease in glutathione levels and activities of superoxide dismutase and an to this increase in indicators, a significant decrease in glutathione levels and activities of superoxide dismutase and an
increase in malondialdehyde level were detected. Biochemical and histopathologic results in the ISO-induced model of myocardial increase in malondialdehyde level were detected. Biochemical and histopathologic results in the ISO-induced model of myocardial
injury emphasize the beneficial action of amiodarone as a cardioprotective agent. injury emphasize the beneficial action of amiodarone as a cardioprotective agent.
Cardiovascular Toxicology 04/2012; 9(4):161-168. · 2.07 Impact Factor
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ABSTRACT: In this study, the anti-inflammatory effects of a tropolone derivative, 2,5-dihydroxycyclohepta-2,4,6-trienone (AD-4), were
investigated. The anti-inflammatory potency of AD-4 was compared with that of indomethacin in carrageenan-induced inflammation
models in rats. The effect on vascular permeability was also determined by hyaluronidase-induced capillary permeability. AD-4
decreased carrageenan-induced paw edema at doses of 3.62×102, 7.24×102, and 14.48×102μmol/kg by 45% (p<0.001), 79% (p<0.001), and 83% (p<0.001), respectively, compared with the value of 49% (p<0.001) for indomethacin (69.8μmol/kg). Additionally, AD-4 decreased hyaluronidase-induced capillary permeability significantly.
In conclusion, AD-4 was determined to have anti-inflammatory effects with lower toxicity than indomethacin. Anti-inflammatory
effect of AD-4 may be related to its effects on vascular permeability.
Medicinal Chemistry Research 04/2012; 19(1):84-93. · 1.27 Impact Factor
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ABSTRACT: Objective: In this study, anticancer effects of mirtazapine on rats were investigated in an adenocarcinoma model induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and compared with those of cisplatin. Materials and Methods: For this purpose, 10 mg/kg doses of mirtazapine were administered orally to one group of rats, while 1 mg/kg doses of cisplatin were administered intraperitoneally to another group. At 1 hour after administration, 200 mg/kg doses of MNNG were given orally to both groups. MNNG administration was repeated once every 10 days through 3 months, after which period, gastric tissue was taken and pathologically evaluated. Results: Mirtazapine prevented adenocarcinoma induction by MNNG in rats to a greater extent than cisplatin. Some of the rats receiving cisplatin demonstrated severe dysplasia in gastric samples and others exhibited mild dysplasia. Rats given mirtazapine were not observed to suffer severe dysplasia, only mild dysplasia being observed. Conclusion: For adenocarcinoma induced by MNNG on rats, mirtazapine was determined more effective than cisplatin. In order to make statement about mechanism of anticancer activity of mirtazapine, wider studies are required.
Asian Pacific journal of cancer prevention: APJCP 01/2012; 13(10):4897-900. · 0.66 Impact Factor
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ABSTRACT: In this study, the effect of mirtazapine on rat kidneys versus ischemia-reperfusion (IR) damage was biochemically and histopathologically investigated. The results have shown that malondialdehyde (MDA) level of healthy rat group is 15.2 mol/g protein. The level of this substance was measured as 26.7 mol/g in only ischemia group. The MDA levels of IR and mirtazapine + renal ischemia-reperfusion (MRIR) groups were 39 ± 17.6 mol/g protein. While myeloperoxidase activity of healthy rat group was 20.2 u/g, the activities of only ischemia, IR, and MRIR groups were 28, 36.3, and 21 u/g, respectively. The glutathione levels were measured as 17.7, 12.8, 7.5, and 16.2 nmol/g in healthy, only ischemia, IR, and MRIR groups, respectively. Finally, glutathione S-transferase activities of healthy, only ischemia, IR, and MRIR groups were determined as 20, 13.8, 7.1, and 18.3 u/g, respectively. Histopathologically, while hemorrhage in interstitial area was observed in only ischemia group, significant tubular epithelial swelling, necrosis, and cast accumulation were seen in IR group. In MRIR group, only mild tubular epithelial swelling and mild hyaline cast accumulation were observed in kidney tissue. Consequently, it can be said that mirtazapine has a protective effect on IR-induced kidney damage.
Renal Failure 01/2012; 34(1):103-10. · 0.82 Impact Factor
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ABSTRACT: To investigate the effects of metyrosine, lacidipine, clonidine, and moxonidine on the renal damage in rats with unilateral ureteral ligation by examining the histological evidence of parenchymal damage and tubular dilatation, as well as biochemical changes indicating cell membrane damage and DNA oxidation.
Thirty-six albino Wistar rats were randomly divided into six equal groups: a healthy (intact) group, a unilateral ureteral ligation (control) group, and four drug treatment groups given metyrosine (50 mg/kg), lacidipine (2 mg/kg), clonidine (0.075 mg/kg), or moxonidine (0.2 mg/kg), respectively, for 10 days. The latter five groups underwent ligation of the left ureter. Ten days after the operation, we removed both kidneys from each rat in the control and drug treatment groups for renal pathological and biochemical [malondialdehyde (MDA), total glutathione, 8-hydroxy-2-deoxyguanine (8-OH-Gua)] examinations. Spectrophotometric assays were used to detect the malondialdehyde and total glutathione levels of the renal tissue. High-performance liquid chromatography was used to measure the 8-hydroxy-2-deoxyguanine levels.
When the drug treatment groups were compared with the control group, the drug treatment groups' total glutathione level was higher and their malondialdehyde level was lower than that of the control group (P < 0.05), especially in the clonidine group (P < 0.0001). The 8-hydroxy-2-deoxyguanine levels of the drug treatment groups, except the lacidipine group, were significantly lower than that of the control group (P < 0.0001). There was no significant difference between the contralateral kidneys of the treatment groups and control group, according to the biochemical results. As revealed via light microscopy, clonidine and moxonidine treatment significantly reduced the tubular and glomerular damage, as well as the tubular dilation. The interstitial inflammation of the kidneys in the lacidipine group was higher than that of the other treatment groups. However, the apoptotic cell count was at a high level in both the lacidipine and metyrosine groups. The increase in the collagen content was most pronounced in the lacidipine and metyrosine groups. An examination of the contralateral kidneys showed no marked pathological findings.
The use of a direct or indirect α2-adrenergic receptor agonist for the temporary treatment of unilateral ureteral obstruction-induced renal damage may be important for preventing renal structural injury. A more advanced study is necessary to determine the mechanisms underlying the protective effects of these drugs with regard to renal damage in ureteral obstruction.
Surgery Today 12/2011; 42(11):1051-60. · 1.22 Impact Factor
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ABSTRACT: In this study, an investigation was performed on the ovarian tissue of rats subjected to ischemia-reperfusion for the effect of famotidine on certain parameters of oxidation-antioxidation, cell DNA damage, and histological appearance.
The effects of famotidine on certain parameters of oxidation-antioxidation (total glutathione [tGSH], superoxide dismutase [SOD], malondialdehyde) and cellular DNA injury in the ovarian tissue of rats subjected to ischemia-reperfusion were investigated and underwent histological examination.
The results show levels of 5.2 ± 0.6 nmol/g protein for tGSH, 8.3 ± 0.8 U/g for SOD activity, and 7.7 ± 0.9 μmol/g protein for malondialdehyde (P < .0001 when compared with controls) in ovarian tissue subjected to ischemia-reperfusion following famotidine treatment. The tGSH levels in control rats and in a healthy animal group were, respectively, 1.76 ± 0.7 and 5.5 ± 0.3 nmol/g protein (P < .0001). The SOD activity was 3.2 ± 0.9 U/g in control and 9.2 ± 0.6 U/g in healthy animal tissues. The differences between the values in the treatment and the control group, and between the healthy animal group and the control group were both highly significant (P < .0001). It was also observed that famotidine prevented, to a significant extent, an increase in the level of 8-hydroxy-2-deoxyguanine/guanine, a DNA damage product, as compared with the control group.
These biochemical and histological results show that famotidine protects the ovarian tissue from ischemia-reperfusion injury.
Journal of Pediatric Surgery 09/2011; 46(9):1817-23. · 1.45 Impact Factor
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ABSTRACT: Some endogenous hormones (epinephrine and cortisol) can change an individual's pain threshold. Propranolol is a non-selective β adrenergic receptor blocker which antagonises the anti-inflammatory effect of non-steroidal anti-inflammatory drugs via the β1 and β2 adrenergic receptors. The roles of epinephrine and cortisol were investigated in the analgesic activity of metyrosine in rats with reduced epinephrine levels induced by metyrosine. Pain threshold measurement was performed using an analgesimeter with different doses and the single or combined usage of metyrosine, prednisolone, metyrapone and propranolol in rats. Epinephrine and corticosterone levels were measured by high-performance liquid chromatography in metyrosineadministered rats. Metyrosine reduces the epinephrine levels without affecting the corticosterone levels, thereby creating an analgesic effect. It was determined that prednisolone did not have an analgesic effect in rats with normal epinephrine levels, but its analgesic activity increased with a parallel decrease in the epinephrine levels. Similarly, the combined use of prednisolone and metyrosine provided a stronger analgesic effect than that rendered by metyrosine alone. The strongest analgesic effect, however, was observed in the group of rats with the lowest epinephrine level in whom the metyrosine + prednisolone combination was administered. The findings of this study may be useful in severe pain cases in which the available analgesics are unable to relieve the individual's pain.
Archives of Pharmacal Research 09/2011; 34(9):1519-25. · 1.59 Impact Factor
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ABSTRACT: It was biochemically and histopathologically investigated whether disulfiram has protective effects on ischemia-induced ovary damage. For this purpose, levels of tGSH, superoxide dismutase (SOD), malondialdehyde (MDA), and 8-OH Gua/Gua were investigated in ischemic rat ovary tissue. Results show that used doses of disulfiram (10, 25, and 50 mg/kg) prevent MDA, a product of ischemia-induced lipid peroxidation, formation in female rat ovary tissue and prevent decrease of enzymatic and non-enzymatic (SOD, GSH) antioxidant parameters. Additionally, all doses of disulfiram significantly prevent DNA damage when compared to control group. Fewer histopathological findings were observed in tissues with higher antioxidant levels and lower oxidant and DNA damage levels.
Gynecological Endocrinology 07/2011; 28(2):143-7. · 1.58 Impact Factor
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ABSTRACT: The rat sepsis model in the present study was used to understand the role of sustained hyperglycemia and ovariectomy, either separately or together, on the response of pro-inflammatory mediators and oxidative response.
Polymicrobial sepsis was induced using cecal ligation and two-hole puncture. Diabetes was induced in the female Wistar albino rats using intraperitoneal administration of aqueous alloxan monohydrate at a single dose of 150 mg/kg body weight. The rats were divided into five groups: sham control: group 1, ovariectomy: group 2, ovariectomy + sepsis: group 3, ovariectomy + diabetes: group 4, and ovariectomy + diabetes + sepsis: group 5.
In lung, heart, and liver tissues, the levels of myeloperoxidase (MPO) and lipid peroxidation (LPO) were higher for the groups 3, 4, and 5 than in control group. In heart and liver tissues, superoxide dismutase (SOD) and catalase (CAT) activities were higher for the groups 3, 4, and 5 than control group. In lung tissue SOD activities were higher for the groups 3, 4, and 5 than in control group. Diabetes + ovariectomy caused a significant increase in serum levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in comparison to the sham group. The strongest production of TNF-α and IL-6 in serum was observed in the group 5.
Hyperglycemia and ovariectomy (postmenopausal period) severely increased serum cytokines and oxidant levels with the stages of our sepsis model. The lung tissue was most affected by diabetes and ovariectomy under sepsis conditions. Ovariectomy leading to estrogen deficiency results in general changes in metabolism, which are seen in the liver, lungs, and heart with diabetes under sepsis conditions.
Journal of Surgical Research 07/2011; 169(1):67-75. · 2.25 Impact Factor
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ABSTRACT: There is limited study about anti-inflammatory effect mechanism of tamoxifen. We aimed to investigate the anti-inflammatory activity of tamoxifen to see whether adrenal gland hormones have roles in the anti-inflammatory effect mechanism of tamoxifen and to evaluate the relationship between anti-inflammatory activity and cyclooxygenase (COX) level.
Effects of tamoxifen, indomethacin and prednisolon on carrageenan-induced inflammatory paw oedema were investigated in intact and adrenalectomised rats. Also blood adrenalin and corticosterone levels and paw tissue COX levels determined biochemically.
Tamoxifen (5, 10 and 20 mg/kg), indomethacin (5, 10 and 20 mg/kg) and prednisolon (5 mg/kg) produced anti-inflammatory effects in intact rats, however, they could not in adrenalectomized rats. 20 mg/kg tamoxifen produced low anti-inflammatory effect. Tamoxifen and indomethacin decreased COX-2 levels in intact rats, but not in adrenalectomised rats. Tamoxifen produced anti-inflammatory effects by decreasing adrenalin levels, as indomethacin does. 20 mg/kg tamoxifen decreased corticosterone levels.
Tamoxifen was seen to suppress carrageenan-induced inflammation significantly. The dose of tamoxifen that decreases adrenalin levels maximally and decreases corticosterone levels minimally was found to produce the most potent anti-inflammatory effect. The reason why indomethacin is more potent in high doses may be that it decreases adrenalin levels strongly at these doses, without decreasing corticosterone levels.
Gynecological Endocrinology 04/2011; 27(4):241-7. · 1.58 Impact Factor
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ABSTRACT: In this study, effects of chronic antihypertensive drug (clonidine, methyldopa, amlodipine, ramipril, and rilmenidine) treatment on antioxidant-oxidant parameters were investigated in rat ovarian tissue.
Chronic drug administration for 30 days and at the end, biochemical examinations (total glutathione (tGSH), glutathione peroxidase (GPO), glutathione reductase (GR), glutathione s-transferase (GST), superoxide dismutase (SOD), nitric oxide (NO), catalase (CAT), malondialdehyde (MDA), and myeloperoxidase (MPO) analyses) were performed.
The levels of glutathione (GSH) and NO, and the activities of GPO, GR, GST, SOD, and CAT were measured the lowest in ramiprile group. Also in ramiprile group, the level of MDA and the activity of MPO was the highest.
We divided the drugs into four groups according to their biochemical side effect potentials in ovarian tissue: (I) Drugs which have no clear negative effect on ovarian tissue: clonidine, rilmenidine; (II) Drugs which have mild negative effect on ovarian tissue: methyldopa; (III) Drugs which have moderate negative effect on ovarian tissue: amlodipine; (IV) Drugs which have severe negative effect on ovarian tissue: ramipril. These data might be useful in the selection of the least toxic antihypertensive drug in pregnant and/or normal females.
Gynecological Endocrinology 01/2011; 27(11):895-9. · 1.58 Impact Factor
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ABSTRACT: We investigated the potential protective effects of montelukast (MLK) on cecal ligation and puncture (CLP)-induced tissue injury in vital organs - liver, heart, kidneys, and especially lungs - through inhibition of the proinflammatory cytokine response and the generation of reactive oxygen species (ROS) in rats. The rat groups were (1) a 10-mg/kg MLK-treated CLP group; (2) a 20-mg/kg MLK-treated CLP group; (3) a 20-mg/kg MLK-treated, sham-operated group; (4) a CLP control group; and (5) a sham-operated control group. MLK treatment significantly decreased proinflammatory (tumor necrosis factor-alpha, interleukin-6) cytokine levels following CLP. The lipid peroxide level increased in the lung, heart, liver, and kidney tissues after CLP-induced sepsis, and myeloperoxidase activity increased in the lung, heart, and liver tissues. MLK attenuated this elevation in all tissues except the kidney, dose dependently. The glutathione levels and superoxide dismutase activity were significantly increased in the lung, liver, and kidney tissues after MLK treatment. MLK treatment after CLP also potentially reduced mortality. The lung and kidney tissues were the most protected by MLK under sepsis conditions. We can suggest that MLK reverses the systemic inflammatory reaction to polymicrobial sepsis and thereby reduces multiple organ failure.
TheScientificWorldJOURNAL 01/2011; 11:1341-56. · 1.66 Impact Factor
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ABSTRACT: α-Lipoic acid (ALA) has been termed the 'ideal' antioxidant, a readily absorbed and bioavailable compound capable of scavenging a number of free radicals, and it has been used for treating diseases in which oxidative stress plays a major role. The present study was designed to gain a better understanding for the positive effects of ALA on the models of acute and chronic inflammation in rats, and also determine its anti-oxidative potency. In an acute model, three doses of ALA (50, 100 and 200 mg/kg) and one dose of indomethacin (25 mg/kg) or diclofenac (25 mg/kg) were administered to rats by oral administration. The paw volumes of the animals were calculated plethysmometrically, and 0·1 ml of 1 % carrageenan (CAR) was injected into the hind paw of each animal 1 h after oral drug administration. The change in paw volume was detected as five replicates every 60 min by plethysmometry. In particular, we investigated the activities of catalase, superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR), inducible NO synthase (iNOS) and myeloperoxidase (MPx), and the amounts of lipid peroxidation (LPO) or total GSH in the paw tissues of CAR-injected rats. We showed that ALA exhibited anti-inflammatory effects on both acute and chronic inflammations, and a strongly anti-oxidative potency on linoleic acid oxidation. Moreover, the administration of CAR induced oedema in the paws. ALA significantly inhibited the ability of CAR to induce: (1) the degree of acute inflammation, (2) the rise in MPx activity, (3) the increases of GST and iNOS activities and the amount of LPO and (4) the decreases of GPx, GR and SOD activities and the amount of GSH. In conclusion, these results suggest that the anti-inflammatory properties of ALA, which has a strong anti-oxidative potency, could be related to its positive effects on the antioxidant system in a variety of tissues in rats.
The British journal of nutrition 11/2010; 105(1):31-43. · 3.45 Impact Factor
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ABSTRACT: The aim of the study was to examine whether endogenous cortisol and adrenalin have a role in the formation of stress ulcers in intact and adrenalectomized rats.
The study was composed of 4 experiments: ulcerated areas in stomachs of adrenalectomized and intact rats were measured, adrenaline (100 μg/kg) and prednisolone (5 mg/kg) were injected intraperitoneally in adrenalectomized rats, metyrapone (200 mg/kg) and metyrosine (200 mg/kg) were administered to intact rats, and metyrapone (200 mg/kg) and metyrosine (200 mg/kg) were administered orally with yohimbine (10 mg/kg) and yohimbine (10 mg/kg) alone were administered to intact rats. After 24-hour restraint stress, ulcerated areas were measured.
In the stomach of intact rats, the degree of stress ulcer was 7.25 times more severe than that noted in adrenalectomized rats. Furthermore, stress ulcers in adrenalectomized rats that received adrenaline or prednisolone only were fewer and less severe than rats receiving both adrenaline and prednisolone.
Simultaneous administration of adrenaline and prednisolone did not prevent the formation of stress ulcers. However, either of these hormones alone (adrenaline or prednisolone), in the absence of the other, repressed the formation of stress ulcers. This antiulcer activity may be related to α2-adrenergic receptor activity.
Journal of Pediatric Surgery 11/2010; 45(11):2154-9. · 1.45 Impact Factor
