X.-H. Li

Third Military Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (12)9.06 Total impact

  • Y. Wang · X.-L. Lu · H. Yang · X.-H. Li · H.-G. Zhang
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    ABSTRACT: OBJECTIVE: To explore the effects of Huilixinkang (HLXK), a mimetic polypeptide of Gq protein carboxyl terminus, on myocardial hypertrophy and expressions of myosin heavy chain (MHC) in mice. METHODS: Sixty mice were randomly divided into 6 groups, ie control, model, losartan and HLXK (10, 30, 90 μg·kg-1) groups; and administrated with normal saline, noradrenaline 1.5 mg·kg-1 (ip, bid), losartan 9 mg·kg-1 and HLXK 10, 30, 90 μg·kg-1 (ip, bid), respectively. After 20 days' treatment, all the mice were killed, and the cardiac hypertrophy indexes including heart weight index and left ventricular mass index were measured. The expressions of α-MHC and β-MHC in myocardium were determined using immunohistochemistry technique. RESULTS: Noradrenaline could induce cardiac hypertrophy in mice significantly. Losartan 9 mg·kg-1, HLXK (30, 90 μg·kg-1) markedly decreased heart weight index and left ventricular mass index, elevated the expression of α-MHC and decreased the expression of β-MHC in myocardium. CONCLUSION: HLXK can effectively prevent cardiac hypertrophy in mice, and balance the expression of myosin heavy chain in the process of myocardial hypertrophy.
    No preview · Article · Oct 2011 · Journal of Chinese Pharmaceutical Sciences
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    L. Y. Hao · X. Q. Hao · S. H. Li · X. H. Li

    Preview · Article · Aug 2010 · Neuroscience
  • L.Y. Hao · X.Q. Hao · S.H. Li · X.H. Li
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    ABSTRACT: Studies have suggested that maternal infection/inflammation maybe a major risk factor for neurodevelopmental brain damage. In the present study, we evaluated the effects of prenatal exposure to a low level of inflammatory stimulation lipopolysaccharide (LPS) repeatedly on spatial learning and memory performances in rat offspring's lifetime. Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups. The rats in the LPS group were treated i.p. with LPS (0.79 mg/kg) at gestation day 8, 10 and 12; meanwhile the rats in the control group were treated with saline. After delivery, the rat offspring at 3- (young), 10- (adult) and 20-mon-old (aged) were allocated. Spatial learning and memory abilities were tested by Morris water maze. The structure of hippocampal CA1 region was observed by light microscopy. The expression of synaptophysin (SYP) and glial fibrillary acidic protein (GFAP) in hippocampal CA1 region were measured by immunohistochemistry. Results showed that the rat offspring of LPS group needed longer escape latency and path-length in the Morris water maze and presented a significant neuron loss, decreased expression of SYP, increased expression of GFAP in CA1 region in histological studies. All these changes were more significant with the age increasing. These findings support the hypothesis that maternal systemic inflammation may alter the state of astrocytes in rat offspring for a long time, the alteration may affect neurons and synapse development in neural system, increase the neurons' vulnerability to environment especially as the age increasing, at last result in distinct learning and memory impairment.
    No preview · Article · Mar 2010 · Neuroscience
  • H. Yang · X.-L. Lu · X.-H. Li · H.-G. Zhang
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    ABSTRACT: Objective: To study the influence of 60Co radiation and heating on anti-cardiac hypertrophy activity of the polypeptide drug (GCIP)-27 , and provide experimental evidence for the choice of best degerming method. Methods: The instability index, aliphatic index, the grand average of hydropathicity, average flexibility and buried residues of peptide GCIP-27 were predicted respectively by bioinformatics tool ProtParam and ProtScale. Observe the influence of 60Co radiation 25 kGy and heating 115°C independently on anti-cardiac hypertrophy activity of GCIP-27 (100 μg·kg-1) when rat modle with cardiac hypertrophy was induced by norepinephrine (NE). Results: The prediction showed that GCIP-27 is a stabile polypeptide and has good thermostability. Compared with the NE control, both radiated drug and heated drug significantly decreased the heart index and left ventricular index in mice, while there was no significant difference between treated drug and untreated drug groups, respectively. Conclusion: Conventional radiation and megatemperature degerming have no harmful influence on anti-cardiac hypertrophy activity of GCIP-27.
    No preview · Article · Jan 2010 · Chinese Journal of New Drugs
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    ABSTRACT: Objective: To determine the effect of G protein competitive inhibitory peptide (GCIP-27) on the right ventricular cardiomyocyte apoptosis induced by monocrotaline (MCT) and the possible mechanism. Methods: Sprague-Dawley rats were randomly divided into 4 groups. Cardiomyocyte apoptosis was induced by MCT, and treated with GCIP-27 (30 or 90 μg·kg-1, ip, bid). On day 22, right ventricular systolic pressure (RVSP) was measured through right heart catheterization. The apoptosis of right ventricular cardiomyocytes was detected by TdT mediated nick dUTP end-labeling (TUNEL) technique in the paraffin-embedded right ventricular tissues. The expression of Bcl-2 and Bax antigens in right ventricular tissues was evaluated by immunohistochemical technique. Results: GCIP-27 significantly inhibited the RVSP (P < 0.05, P < 0.01) and reduced the right ventricular cardiomyocyte apoptosis(P < 0.01). GCIP-27 markedly improved MCT-induced Bax over-expression and Bcl-2 low-expression in right ventricular cardiomyocytes (P < 0.01). Conclusion: GCIP-27 can attenuate MCT-induced apoptosis of right ventricular cardiomyocytes in rats; the mechanism may be associated with the up-regulation of Bcl-2 and down-regulation of Bax as well as the reduction in RVSP.
    No preview · Article · Aug 2009 · Chinese Journal of New Drugs
  • D.-L. Yang · X.-H. Li · H.-G. Zhang · X.-J. Yang · X.-Q. Hao · M. Su
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    ABSTRACT: OBJECTIVE: To explore the effect and the preliminary mechanism of cyclosporine A (CsA) on the right ventricle remodeling caused by monocrotaline (MCT). METHODS: Thirty-six Sprague-Dawley male rats were randomly divided into normal control group, MCT group, low and high dose of CsA treatment group. Rats were given a single dose of MCT (50 mg·kg-1, sc) for inducing the right ventricle remodeling. CsA (0.33 and 1 mg·kg-1, bid, ig) was administered from day 14 to day 21 respectively. The right ventricle (RV) and the left ventricle with septum (LV+SEP) were weighed separately. RVHI was measured as RV/(LV+SEP). The histological examination of RV were executed by light microscope. The ultramicrostructure of the RV tissues was observed under the transmission electron microscope. Immunohistochemical analysis was performed on paraffin-embedded RV tissue using the anti-proliferating cell nuclear antigen (PCNA) primary antibodies. RESULTS: CsA significantly inhibited the increase of RV systolic pressure and RVHI, compared with MCT group (P<0.05 or P<0.01). Histological examination revealed that CsA effectively prevented RV cardiomyocytes hypertrophy. The transmission electron microscope examination demonstrated that the swollen and misshapen mitochondria in RV cardiomyocytes induced by MCT was improved by CsA. CsA effectively reduced the PCNA expression in RV cardiomyocytes. The effect of high dose CsA was more significant (P<0.01). CONCLUSION: CsA (1 mg·kg-1, ig, bid) can improve the RV remodeling effectively in MCT- treated rats. The mechanism may be related to the reduction of RV systolic pressure and the inhibition of the cardiac hypertrophy.
    No preview · Article · Jul 2009 · Journal of Chinese Pharmaceutical Sciences
  • Z B Yuan · H G Zhang · Y Jia · Y Q Cheng · X H Li
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    ABSTRACT: To explore the temporal expression pattern of cyclooxygenase (COX)-2 and effects of panax notogensing saponins (PNS) in peritoneal macrophages of rats. Phagocytosis function of peritoneal macrophages was measured by chicken red blood cell phagocytosis assay in vitro. Expression of COX-2 mRNA and protein, PGE(2) and PGD(2) production were determined with real-time PCR, Western blotting and radioimmunoassay, respectively. Phagocytosis function of macrophages increased significantly after stimulation and reached peak during 2-3h. Expression of COX-2 mRNA and its protein increased markedly after stimulation and reached the first peak at 2 h and 3h, respectively; and then decreased to reach a minimum at 24h. The second peak appeared at 36h. PNS (50, 100, 200 mg/kg) increased the phagocytosis function obviously at 2h, decreased the expression level of COX-2 and PGE(2) production at 2 h and elevated COX-2 expression and PGD(2) production at 36 h, respectively. COX-2 expression in peritoneal macrophages has a double-hump feature after stimulation. PNS enhanced phagocytosis, inhibiting COX-2 expression at an early stage and elevating it at a later stage.
    No preview · Article · Mar 2009 · Agents and Actions
  • D.-L. Yang · X.-H. Li · H.-G. Zhang · X.-J. Yang · X.-Q. Hao · M. Su
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    ABSTRACT: Aim: The effect and mechanism of GCIP-27 on the right ventricle remodeling by monocrotaline (MCT) were explored. Methods: Sprague-Dawley rats were randomly divided into the normal group, MCT group and the low and high dose GCIP-27 treatment group. Pulmonary arterial systolic pressure (PASP), pulmonary artery diastolic pressure (PADP) and mean pulmonary arterial pressure (MPAP) were measured by right cardiac catheter on the 22 th day. RV and left ventricle plus septum were weighed separately. Right ventricular hypertrophy index (RVHI) was measured by the weight ratio of RV to left ventricle plus septum. The histological examination of right ventricle were executed by light microscope and transmission electron microscope. Immunohistochemical analysis was performed on the paraffin-embedded right ventricle tissue using the anti-PCNA primary antibodies. Results: GCIP-27 (90 μg · kg-1) significantly inhibited the progression of PASP and MPAP and GCIP-27 (30 μg · kg-1) only reduced the progression of PASP. GCIP-27 significantly inhibited the increase of RVHI and cardiomyocytes hypertrophy versus MCT group. The swollen and misshapen mitochondria could be improved by GCIP-27. And the PCNA expression caused by MCT could be inhibited by GCIP-27 in right ventricle cardiomyocytes. Conclusion: GCIP-27 can attenuate the right ventricular remodeling siginificantly in monocrotaline-treated rats.
    No preview · Article · Dec 2008 · Chinese Pharmacological Bulletin
  • X.-Q. Wang · X.-H. Li · H.-G. Zhang · D.-L. Yang
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    ABSTRACT: OBJECTIVE: To develop an isotope tracing method for the pharmacokinetics of GCIP-27 in mice. METHODS: 125I-GCIP was prepared by lodogen method. Isotope tracing method combined with trichloroacetic acid (TCA) precipitation and low molecular weight SDS-PAGE method were used to determine GCIP-27 in mice plasma. RESULTS: TCA method and SDS-PAGE method were used to measure the concentration of 60 mouse plasma samples. There was a good linear correlation (r = 0.955 4) between the two methods. Within-day and between-day precision were less than 10%. Their linearities were determined in the range of 3.75-480 μg·L-1 in plasma (r = 0.997 7 and 0.996 4, respectively). The average recoveries of the two methods of GCIP were (92.72 ± 4.55) and (91.77 ± 5.21)%, respectively. CONCLUSION: Both the methods are stable, reliable and sensitive. They are suitable for the determination of GCIP concentration in mice plasma.
    No preview · Article · May 2008 · Journal of Chinese Pharmaceutical Sciences
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    ABSTRACT: Objective: To explore the effect and the mechanism of cyclosporine A (CsA) on pulmonary hypertension induced by monocrotaline(MCT) in rats. Methods: Thirty six Sprague-Dawley male rats were randomly divided into normal control group (n=8), MCT model group (n=12), low dose CsA (0.33 mg·kg-1) (n=8) and high dose CsA group (n = 8). A single dose of MCT (50 mg·kg-1) was subcutaneously injected to induce pulmonary hypertension. CsA was administered 14-21 days after MCT injection when pulmonary hypertension had already been established. Hemodynamic parameters were measured by Powerlab on day 22. The heart was separated into the right ventricle (RV) and the left ventricle with septum, and weighed separately. RVHI was measured as RV/ (LV+septum); the lung weight (LW)/body weight (BW) were calculated. Left lung leafs were stained with haematoxylin-eosin, and examined under a light microscope. Immunohistochemical analysis was performed on paraffin-embedded left lung tissue using the anti-PCNA (proliferating cell nuclear antigen) primary antibody. Results: CsA (0.33 and 1 mg·kg-1) significantly inhibited the progression of pulmonary artery pressure, the increase of the RVHI and the ratio of lung weight/body weight (P < 0.05 or P < 0.01) after MCT-induced pulmonary hypertension. Histological examination revealed that CsA effectively prevented pulmonary arterial medial thickening (P < 0.05 or P < 0.01), and attenuated inflammation. CsA effectively reduced the PCNA expression in pulmonary artery smooth muscle cells (PASMC) (P < 0.05 or P < 0.01). The effects of 1 mg·kg-1 CSA were more significant. Conclusions: CsA reverses the development of pulmonary hypertension induced by MCT in rats. The mechanism may be related to reduction of the proliferation of PASMC and inhibition of the lung inflammation.
    No preview · Article · Jan 2008 · Chinese Journal of New Drugs
  • X.-Q. Wang · X.-H. Li · H.-G. Zhang · Y.-Q. Cheng
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    ABSTRACT: Aim: To observe the effects of GCIP-27 (G protein competitive inhibitory polypeptide-27) on the structure of left ventricle in spontaneously hypertensive rats (SHR). Methods: Thirty SHR rats of 12 weeks old were randomly divided into five groups (n = 6): blank control groups, GCIP-27 (10,30,90 μg·kg-1, ip, bid) groups, and Losartan group (6 mg·kg-1), six Wistar-Kyotos (WKY) rats were as normal control. Systolic blood pressure (SBP) was measured once per two weeks with tail-sleeve methods. At the end of the 8th week, left ventricle weight index (LVWI) were determined. Myocardium structure was observed by polaroscope and transmission electron microscope. The area and content of myocardial interstitial collagen were treated for semiquantitative analysis by image analyzer system. Results: The SBP in GCIP-27 (10,30,90 μg ·kg-1) groups decreased significantly from the 2 nd to the 8th week by comparison with blank control group. GCIP-27 (10,30,90 μ·kg-1) lowered heart mass index (HMI) and left ventricular mass index (LVMI) markedly compared with blank control group (P < 0.05). Collagen area (CA), integral optic density (IOD) and collagen volume fraction (CVF) of myocardial interstitial in the GCIP-27 (10,30,90 μg·kg-1) groups were lowered compared with those in the control group (P < 0.01). GCIP-27 was more obvious in improving myocardial ultrastructure and pathology such as hypertrophy and degeneration. Conclusions: GCIP-27 plays a preventive and protective role in the development of left ventricular remodeling of spontaneously hypertensive rats. It can improve the myocardial structure, attenuate the hyperplasia of collagen markedly, and reduce the blood pressure as well.
    No preview · Article · Aug 2007
  • J.Z. Zhou · X.H. Li · H.G. Zhang · Y. Tang · X.Q. Wang

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