AIM： To evaluate the effects of osthole on fatty liver, and investigate the possible mechanism. METHODS： A quail model with hyperlipidemic fatty liver and rat model with alcoholic fatty liver were set up by feeding ...AIM： To evaluate the effects of osthole on fatty liver, and investigate the possible mechanism. METHODS： A quail model with hyperlipidemic fatty liver and rat model with alcoholic fatty liver were set up by feeding high fat diet and alcohol, respectively. These experimental animals were then treated with osthole 5-20 mg/kg for 6 wk, respectively. Whereafter, the lipid in serum and hepatic tissue, and coefficient of hepatic weight were measured. RESULTS： After treatment with osthole the levels of serum total cholesterol （TC）, triglyceride （TG）, lower density lipoprotein-cholesterol （LDL-C）, coefficient of hepatic weight, and the hepatic tissue contents of TC and TG were significantly decreased. The activity of superoxide dismutase （SOD） in liver was improved. In alcohol-induced fatty liver rats, the level of malondialdehyde （MDA） in liver was decreased. In high fat-induced fatty liver quails, glutathione peroxidase （GSH-PX） in liver was significantly improved. The histological evaluation of liver specimens demonstrated that the osthole dramatically decreased lipid accumulation. CONCLUSION： These results suggested that osthole had therapeutic effects on both alcohol and high fatinduced fatty liver. The mechanism might be associated with its antioxidation.展开更多
AIM： To observe the anti-liver fibrosis effect of Astragalus complanatus fiavonoids （ACF） in rats. METHODS： The liver fibrosis model in rats was established by injecting interperitoneally 0.2 mL/100 g 0.5% dimethy...AIM： To observe the anti-liver fibrosis effect of Astragalus complanatus fiavonoids （ACF） in rats. METHODS： The liver fibrosis model in rats was established by injecting interperitoneally 0.2 mL/100 g 0.5% dimethylnitrosamine, thrice a week. Meanwhile, the rats were administered ACF （30, 60, 120 mg/kg） or colchicine （0.1 mg/kg） once a day for 1 mo. Serum N-propeptide of type Ⅰ procollagen （PINP） and type Ⅲ procollagen （PⅢNP） was measured using ELISA. Malondialdehyde （MDA） and superoxide dismutase （SOD） in hepatic tissue were evaluated. Matrix metal protease-1 （MMP-1） mRNA expression was assayed by RT-PCR and the protein expression of tissue inhibitor of metal protease-1 （TIMP-1） was analyzed by immunohistochemistry. RESULTS： In the ACF groups, SOD activity increased and MDA content decreased in comparison to the liver fibrosis model group. The serum PINP and PⅢNP contents in ACF-2 and -3 group decreased compared to those in model group. In ACF-2 and -3 group, the expression of MMP-1 mRNA increased significantly and the protein expression of TIMP-1 decreased compared to that in model group. CONCLUSION： The antifibrotic mechanisms of ACF are associated with its influence on lipid peroxidation and collagen synthesis and degradation.展开更多
Objective To investigate the analgesia induced by cobrotoxin （CT） from venom of Naja naja atra, and the effects of atropine and naloxone on the antinociceptive activity of CT in rodent pain models. Methods CT was ad...Objective To investigate the analgesia induced by cobrotoxin （CT） from venom of Naja naja atra, and the effects of atropine and naloxone on the antinociceptive activity of CT in rodent pain models. Methods CT was administered intraperitoneally （33.3, 50, 75 μg/kg）, intra-cerebral venticularly （2.4 μg/kg） or microinjected into periaqueductal gray （PAG, 1.2 μg/kg）. The antinociceptive action was tested using the hot-plate test and the acetic acid writhing test in mice and rats. The involvement of cholinergic system and the opioid system in CT-induced analgesia was examined by pretreatment of animals with atropine （0.5 mg/kg, im or 10 mg/kg, ip） or naloxone （3 mg/kg, ip）. The effect of CT on motor activity was tested using the Animex test. Results CT （33.3, 50 and 75 μg/kg, ip） exhibited a dosedependent analgesic action in mice as determined with hot-plate test and acetic acid writhing test. In the mouse acetic acid writhing test, the intra-cerebral ventricle administration of CT 2.4 μg/kg （1/23th of a systemic dose） produced marked analgesic effects. Microinjection of CT 1.2 μg/kg （1/46th of systemic dose） into the PAG also elicited a robust analgesic action in the hot-plate test in rats. Atropine at 0.5 mg/kg （ira） or naloxone at 3 mg/kg （ip） failed to block the analgesic effects of CT, but atropine at 10 mg/kg （ip） did antagonize the analgesia mediated by CT in the mouse acetic acid writhing test. At the highest effective dose of antinociception （75 μg/kg）, CT did not change the spontaneous mobility of mice. Conclusion These results suggest that CT from Naja naja atra venom has analgesic effects. Central nervous system may be involved in CT＇ analgesic effects and the PAG may be the primary central site where CT exerts its effects. The central cholinergic system but not opioid system appears to be involved in the antinociceptive action of CT.展开更多
Huntington disease （HD） is a chronic autosomal-dominant neurodegenerative disease. The gene coding Huntingtin has been identified, but the pathogenic mechanisms of the disease are still not fully understood. This pa...Huntington disease （HD） is a chronic autosomal-dominant neurodegenerative disease. The gene coding Huntingtin has been identified, but the pathogenic mechanisms of the disease are still not fully understood. This paper reviews the involvement of mitochondrial dysfunction in pathogenesis of HD.展开更多
文摘AIM： To evaluate the effects of osthole on fatty liver, and investigate the possible mechanism. METHODS： A quail model with hyperlipidemic fatty liver and rat model with alcoholic fatty liver were set up by feeding high fat diet and alcohol, respectively. These experimental animals were then treated with osthole 5-20 mg/kg for 6 wk, respectively. Whereafter, the lipid in serum and hepatic tissue, and coefficient of hepatic weight were measured. RESULTS： After treatment with osthole the levels of serum total cholesterol （TC）, triglyceride （TG）, lower density lipoprotein-cholesterol （LDL-C）, coefficient of hepatic weight, and the hepatic tissue contents of TC and TG were significantly decreased. The activity of superoxide dismutase （SOD） in liver was improved. In alcohol-induced fatty liver rats, the level of malondialdehyde （MDA） in liver was decreased. In high fat-induced fatty liver quails, glutathione peroxidase （GSH-PX） in liver was significantly improved. The histological evaluation of liver specimens demonstrated that the osthole dramatically decreased lipid accumulation. CONCLUSION： These results suggested that osthole had therapeutic effects on both alcohol and high fatinduced fatty liver. The mechanism might be associated with its antioxidation.
文摘AIM： To observe the anti-liver fibrosis effect of Astragalus complanatus fiavonoids （ACF） in rats. METHODS： The liver fibrosis model in rats was established by injecting interperitoneally 0.2 mL/100 g 0.5% dimethylnitrosamine, thrice a week. Meanwhile, the rats were administered ACF （30, 60, 120 mg/kg） or colchicine （0.1 mg/kg） once a day for 1 mo. Serum N-propeptide of type Ⅰ procollagen （PINP） and type Ⅲ procollagen （PⅢNP） was measured using ELISA. Malondialdehyde （MDA） and superoxide dismutase （SOD） in hepatic tissue were evaluated. Matrix metal protease-1 （MMP-1） mRNA expression was assayed by RT-PCR and the protein expression of tissue inhibitor of metal protease-1 （TIMP-1） was analyzed by immunohistochemistry. RESULTS： In the ACF groups, SOD activity increased and MDA content decreased in comparison to the liver fibrosis model group. The serum PINP and PⅢNP contents in ACF-2 and -3 group decreased compared to those in model group. In ACF-2 and -3 group, the expression of MMP-1 mRNA increased significantly and the protein expression of TIMP-1 decreased compared to that in model group. CONCLUSION： The antifibrotic mechanisms of ACF are associated with its influence on lipid peroxidation and collagen synthesis and degradation.
文摘Objective To investigate the analgesia induced by cobrotoxin （CT） from venom of Naja naja atra, and the effects of atropine and naloxone on the antinociceptive activity of CT in rodent pain models. Methods CT was administered intraperitoneally （33.3, 50, 75 μg/kg）, intra-cerebral venticularly （2.4 μg/kg） or microinjected into periaqueductal gray （PAG, 1.2 μg/kg）. The antinociceptive action was tested using the hot-plate test and the acetic acid writhing test in mice and rats. The involvement of cholinergic system and the opioid system in CT-induced analgesia was examined by pretreatment of animals with atropine （0.5 mg/kg, im or 10 mg/kg, ip） or naloxone （3 mg/kg, ip）. The effect of CT on motor activity was tested using the Animex test. Results CT （33.3, 50 and 75 μg/kg, ip） exhibited a dosedependent analgesic action in mice as determined with hot-plate test and acetic acid writhing test. In the mouse acetic acid writhing test, the intra-cerebral ventricle administration of CT 2.4 μg/kg （1/23th of a systemic dose） produced marked analgesic effects. Microinjection of CT 1.2 μg/kg （1/46th of systemic dose） into the PAG also elicited a robust analgesic action in the hot-plate test in rats. Atropine at 0.5 mg/kg （ira） or naloxone at 3 mg/kg （ip） failed to block the analgesic effects of CT, but atropine at 10 mg/kg （ip） did antagonize the analgesia mediated by CT in the mouse acetic acid writhing test. At the highest effective dose of antinociception （75 μg/kg）, CT did not change the spontaneous mobility of mice. Conclusion These results suggest that CT from Naja naja atra venom has analgesic effects. Central nervous system may be involved in CT＇ analgesic effects and the PAG may be the primary central site where CT exerts its effects. The central cholinergic system but not opioid system appears to be involved in the antinociceptive action of CT.
文摘Huntington disease （HD） is a chronic autosomal-dominant neurodegenerative disease. The gene coding Huntingtin has been identified, but the pathogenic mechanisms of the disease are still not fully understood. This paper reviews the involvement of mitochondrial dysfunction in pathogenesis of HD.
