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Biomedical subjects

Y M Xin

Publications and source records attributed to Y M Xin.

9 recordsLinked to original sources
PubMed2001

Effects of repeated +Gz exposures on lipid peroxidation of various organs in rats.

OBJECTIVE: To investigate the change of lipid peroxidation in various organs of rats after repeated +10 Gz stress. METHOD: Twenty male Wistar rats were randomly divided into control (+1 Gz) group and +10 Gz group (n = 10 for each group ). The two groups were exposed to +1 Gz or +10 Gz on an animal centrifuge respectively. The onset rate of +Gz was 0.5 G/s; the sustained time at peak +Gz was 30 s each time, with 5 times/d, 1 min intervals, 3 d/wk, 3 wk in total. The rats were decapitated in ice bath on the next day after the last +Gz exposure. The lung, heart, liver and kidney of rats were collected for the following determinations. These organs were made into homogenates and the mitochondria of heart and kidney were isolated from their homogenates. Then malondialdehyde (MDA) content , superoxide dismutase (SOD) activity and glutathion (GSH) concentration in these homogenates and mitochondria were determined individually. RESULT: Compared with the control, MDA concentration in myocardial mitochondria increased significantly (P < 0.01) after repeated +10 Gz exposures, and the SOD activity in liver homogenate and renal mitochondria decreased remarkably (P < 0. 01). But there was no significant difference between GSH concentrations of the two groups. CONCLUSION: Repeated +10 Gz stress induced lipid peroxidation injury of myocardial mitochondria and had some influences on the oxygen radical metabolism of liver and kidney in rats.

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PubMed2001

Protective effects of tea polyphenols on myocardial free radical metabolic disorder in mice induced by inhalation of pure oxygen under 5500 m hypobaric condition.

OBJECTIVE: To observe the protective effects of natural antioxidant tea polyphenols(TP) on myocardial free radical metabolic disorder in mice induced by inhalation of hypobaric pure oxygen under 5500 m hypobaric condition. METHOD: Forty-two male Kunming mice were randomly divided into three groups (n = 14 each): group A, normal control; group B, inhalation of pure oxygen (> 96 %) at simulated altitude of 5500 m in an animal altitude chamber; group C (TP protection group), same as group B but 100 mg/kg of TP was given orally before the exposure. The exposure time was 2 h/d, 3 d/wk for a total of 8 wk, and distilled water was given to groups A and B before exposure. After experiment, the mice were decapitated on the next day and the heart was quickly removed. Malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity and nitric oxide (NO) content were measured. In addition, Cu, Zn-SOD and inducible NO synthase (iNOS) enzymatic contents in myocardial tissue were qualitatively examined by immunohistochemical assaying. RESULT: Compared with the control, MDA concentration, SOD activity and Cu, Zn-SOD enzymatic content in group B were significantly increased (P < 0. 05). But in TP protection group, myocardial MDA formation was significantly decreased (P < 0. 01) and SOD activity and Cu, Zn-SOD expression restored to normal. On the contrary, myocardial NO generation and iNOS expression were significantly reduced after repeated inhalation of hypobaric oxygen at 5500 m. NO metabolism regained to normal after repeated administration of TP. CONCLUSION: Natural antioxidant TP had protective effects on myocardial free radical metabolic disorder induced by inhalation of hypobaric pure oxygen under 5500 m hypobaric condition.

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PubMed2001

[Inhibitory effects of tea polyphenols and vitamin C on lipid peroxidation induced by FeSO4- cysteine in isolated human plasma and carbon tetrachloride-induced liver free radical injury in mice].

OBJECTIVE: To investigate the inhibitory effects of tea polyphenols (TP) and Vitamin C (Vit C) on FeSO4-cysteine induced lipid peroxidation in isolated human plasma and carbon tetrachloride (CCl4) induced liver free radical injury in mice. METHOD: The experiment included two parts: (1) In FeSO4-cysteine induced lipid peroxidation system of isolated human plasma, malondialdehyde (MDA) content was detected after administration of different concentrations of TP (0.3 ~ 8.1 mg/L, as C ~ F group) and Vit C (3 ~ 81 mg/L, as G ~ J group) respectively; (2) Thirty-six male Kunming mice were randomly divided into four groups: control group (A), CCl4 damage group (B), TP protection group (C) and Vit C protection group (D). TP or Vit C (100 mg/kg) was given orally to group C and D respectively, while the same volume of distilled water was given to the other two groups one time every day, continued for three days. Twelve hours after the final treatment, CCl4 (230 mg/kg) was given orally to group B ~ D. Thirty six hours later, all the mice were decapitated and liver homogenate were prepared for measuring MDA content. RESULT: In FeSO4-cysteine induced lipid peroxidation in isolated human plasma, the inhibitory rate of TP (0.3 ~ 8.1 mg/L) was 30.7%, 32.0%, 46.9% and 59.7 %, and the inhibitory rate of Vit C (3 ~ 8.1 mg/L) was 8.3%, 41.4%, 47.7% and 52.7% for various dosages. In the CCl4 induced liver free radical injury system, the inhibitory rate of the same dosage of TP and Vit C was 45.2%, 42.8% respectively. CONCLUSION: TP (0.3 ~ 8.1 mg/L) and Vit C (9 ~ 81 mg/L) had inhibited lipid peroxidation induced by FeSO4-cysteine in isolated human plasma significantly, and the inhibitory effects of TP was superior to that of Vit C at the same dosages. The same dosage of TP and Vit C had remarkable inhibitory effects on the CCl4 induced liver free radical injury, but there was no significant difference between the two groups.

Animals↗
PubMed2001

Protective effects of tea polyphenols on mild hypobaric hypoxia induced pulmonary free radical metabolic disorder in mice.

Objective. To observe the protective effects of natural antioxidant tea polyphenols (TP) on repeated mild hypobaric hypoxia induced pulmonary free radical metabolic disorder in mice. Method. Fourty-two male Kunming mice were randomly divided into three groups (n=14 each): normal control (A); 1500 in mild hypobaric hypoxia (B) and TP protection group (C). The exposure time in hypobaric chamber was 2 h/d, 3d/wk, 8 wk in total. Before hypoxic exposure, TP was orally given to group C at a dose of 100 mg/kg, while distilled water was given to the other two groups. After experiment, the mice were decapitated on the next day and the lung was quickly removed. The malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity and nitric oxide (NO) content were measured. In addition, Cu, Zn-SOD and inducible NO synthase (iNOS) enzymatic contents in lung were were qualitatively examined by immunohistochemical assaying. Result. Compared with the control group, pulmonary MDA concentration and NO content were significantly increased after chronic mild hypobaric hypoxic exposures (P<0.01) but the MDA formation and NO generation in TP protection group were restored to normal. Pulmonary SOD activity in group B tended to increase. Cu, Zn-SOD expression in endothelial cells of bronchioli and iNOS contents in endothelial cells of bronchioli and endothelial cells and smooth muscle cells in pulmonary interstitial vessels were significantly elevated after repeated mild hypobaric hypoxic exposure. These enzymatic abnormal expressions regained to normal after administration of TP. Conclusion. Natural antioxidant TP had protective effects on repeated mild hypobaric hypoxia induced pulmonary free radical metabolic disorder.

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PubMed2001

[Effects of repeated high +Gz exposure on several enzyme activities in cardiomyocytes in rats and some protective measures].

Objective. To determine the changes of several myocardial enzymes in rats after repeated high +Gz exposure and the protective effects of preconditioning of low-G exposure and tea polyphenols (TP). Method. Thirty-two male Wistar rats were randomly divided into 4 groups (n = 8 each): control group (group A), +10 Gz group (group B), low-G preconditioning group (group C) and TP protection group (group D). Group B, C and D were exposed to repeated +10 Gz stress (each for 30s, 5 times/d with +1 Gz 1 min intervals, 3 d/wk, 3 weeks in total), but group A was only submitted to +1 Gz for 5 min. Group C was exposed to +2 Gz for 5 min about 1 h prior to +10 Gz stress. Additionally, TP (200 mg/kg) was given orally to group D about 1 h prior to the +Gz experiment, while distilled water was given to groups A, B and C instead. On the next day after the last centrifuge run, the hearts were taken out immediately for making frozen tissue sections. Enzyme histochemical staining and image analysis were carried out for acid phosphatase (ACP), succinate dehydrogenase (SDH), cytochromeoxidase (Cyt aa3) and adenosine triphosphatase (ATPase). Result. As compared with the control, the activities of ACP and SDH in +10 Gz stressed rats decreased significantly (P<0.05), and there was a declining trend for Cyt aa3. But, low-G preconditioning and TP had protective effects on +10 Gz stress-induced reduction of these enzymatic activities (P<0.05). Conclusion. The results showed that repeated high +Gz exposure could bring about decreases of activities in ACP (the marker enzyme of lysosome) and SDH (the marker enzyme of mitochondrial endomembrane), which indicated a reduction of oxidative metabolism in myocardial tissue; but preconditioning with low-G and natural antioxidant TP had protective effects.

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PubMed1999

Effects of tea polyphenols on cerebral lipid peroxidation, liver and renal functions in rats after repeated +Gz stress.

OBJECTIVE: To observe the effects of repeated +10 Gz stress on cerebral lipid peroxidation, liver and renal function in rats and the prophylactic effects of antioxidant tea polyphenols (TP). METHOD: Twenty-four male Wistar rats were randomly divided into three groups (n = 8, each): group A (control), group B (+10 Gz), and group C (TP). Group B and C were exposed to repeated +10 Gz stress (each for 30s, onset rate about 0.5 G/s, 3 times/d with +1 Gz 1 min intervals, 3 d/wk, 4 weeks in total), but group A was only submitted to +1 Gz. TP (200 mg/kg) was given orally in group C about 1 h prior to the +Gz experiment, while distilled water was given in group A and B. Lipid peroxidation in the brain, liver and renal functions and serum lipids were determined. RESULTS: As compared with the control, lipid peroxidation in rat cerebral homogenate, mitochondria and cytoplasm was significantly increased (P < 0. 05), and serum creatinine concentration was markedly elevated after repeated +10 Gz stress (P < 0. 01). But, TP had significant inhibitory effect on +10 Gz stress induced peroxidative injury in rat brain and reduced the serum creatinine level. There were no differences of serum triglyceride and total cholesterol concentrations and glutamic-pyruvic transaminase activity among the three groups. CONCLUSION: These results indicated that repeated high +Gz stress could bring about peroxidative injury in brain and harmful effect on renal function, and natural antioxidant TP had significant protective effects.

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PubMed1999

Effects of tea polyphenols on cardiac function and myocardial ultrastructure in rats after repeated +Gz stress.

Objective. To observe the effects of tea polyphenols (TP) on cardiac function and myocardial ultrastructure in rats after repeated +10 Gz stress. Method. Twenty four male Wistar rats were randomly divided into three groups (n=8 each): group A (control), group B (+10 Gz), group C (+Gz with TP). Group B and C were repeatedly exposed to +10 Gz (each for 30 s, onset rate about 0.5 G/s, 3 times/d with +1 Gz 1 min intervals, 3 d/wk, 4 weeks in total), but group A was only submitted to +1 Gz. TP (200 mg kg-1) was given orally to group C about 1 h prior to the +Gz experiment, and distilled water was given to group A and B. Function of isolated rat working hearts and myocardial ultrastructure were observed. Result. A significant decrease of left ventricular systolic pressure (LVSP) and injury of myocardial structure in rats were demonstrated after repeated +10 Gz stress. But TP could remarkably elevate the LVSP and improve myocardial ultrastructural injury in +10 Gz stressed rats. Conclusion. These results indicated that repeated high G exposure may produce cardiac structural and functional injuries in rats which might be partly related to free radical metabolism; and antioxidant TP had significant protective effects on the hearts of +Gz stressed rats.

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PubMed1999

[Effects of simulated flight hypobaric hypoxia and oxygen inhalation on free radical metabolism in various organs of mice].

Objective. To investigate the effects of two types of simulated flight conditions (hypobaric hypoxia and hypobaric oxygen inhalation) on free radical metabolism in various organs of mice. Method. Sixty male Kunming mice were randomly divided into six groups (n=10 each). The experiment comprises two parts. The first part included three groups: normal controls (A1), 1500 m hypobaric hypoxia for 4 wk (B1) and 8 wk (C1). The second part included another three groups: normal control (A2), 5500 m hypobaric oxygen inhalation for 4 wk (B2) and 8 wk (C2). The exposure time in hypobaric chamber was 2 h/d, 3 d/wk. After experiment, caudal blood was taken for routine examination. The mice were decapitated on the next day and brain, heart, lung, liver and kidney homogenates were prepared for measuring malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. Result. Lipid peroxides in lung was significantly increased in C1 group, and the content of myocardial MDA and myocardial SOD activities in C2 group were markedly higher than those in A2 group. There were no significant differences among body weights, mean corpuscular indices and hemoglobin content in the normal control, hypobaric hypoxia and hypobaric oxygen inhalation groups. It demonstrates that repeated mild hypobaric hypoxia for 8 wk causes free radical damage of lung and repeated exposure to 5500 m hypobaric oxygen inhalation for 8 wk may lead to myocardial peroxidative injury in mice. Conclusion. Simulated flight hypobaric hypoxia and oxygen inhalation may lead to free radicals damage of lung and myocardial peroxidative injury in mice.

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