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目的:研究玉郎伞黄酮(YLSF)对四氯化碳(carbon tetrachloride,CCl4)所致大鼠肝纤维化的治疗作用,并探讨其作用机制。方法:将SD大鼠随机分成模型组及空白对照组(NC),模型组以50%CCl4食用油溶液为诱导剂ig造模,NC组以生理盐水ig。将病理检查确认形成肝纤维化的SD大鼠,随机分成模型对照组(MC)和药物干预组。药物干预组分别以YLSF(20,40,80 mg.kg-1)及秋水仙碱片(0.20 mg.kg-1)ig;MC组以等剂量生理盐水ig。末次给药24 h后处死大鼠,采集血清及肝组织,检测大鼠血清中天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)活性,测定肝组织中超氧化物岐化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)和谷胱甘肽过氧化酶(GSH-Px),并观察肝组织病理学改变。结果:YLSF(20,40,80 mg.kg-1)各剂量组大鼠血清中AST和ALT分别为(207.85±101.72),(131.55±35.09),(129.98±37.21)U.L-1和(90.51±44.24),(47.79±16.11),(44.56±16.31)U.L-1;YLSF各剂量组大鼠肝组织中SOD,MDA,GSH-Px,GSH含量分别为(143.14±42.82),(146.53±31.98),(147.41±32.82)U.mg-1,(2.57±0.54),(2.19±0.57),(2.11±0.59)nmol.mg-1,(463.55±271.07),(659.14±162.23),(752.08±200.70)nmol.mg-1,(5.06±1.09),(6.10±0.97),(6.89±0.98)nmol.mg-1。各剂量YLSF和阳性药能显著降低大鼠血清中AST(P<0.01)及肝组织MDA含量(P<0.05或P<0.01),并显著提高肝组织中SOD含量(P<0.05或P<0.01);中、高剂量YLSF和阳性药可降低大鼠血清中ALT水平(P<0.01),显著升高大鼠肝组织GSH含量(P<0.01);中、高剂量YLSF能显著升高大鼠肝组织GSH-Px(P<0.01)。各剂量YLSF及阳性药均能够减轻肝细胞损伤程度(P<0.05或P<0.01)。结论:玉郎伞黄酮对CCl4诱导的大鼠具有一定治疗作用,其机制可能与其清除自由基、抑制脂质过氧化有关系。
Objective: To investigate the therapeutic effect of YLSF on liver fibrosis induced by carbon tetrachloride (CCl4) in rats and its mechanism. Methods: SD rats were randomly divided into model group and blank control group (NC). The model group was induced with 50% CCl4 oil solution as the inducer, and the NC group was given physiological saline ig. Pathological examination confirmed the formation of liver fibrosis in SD rats were randomly divided into model control group (MC) and drug intervention group. Drug-intervention groups were treated with YLSF (20, 40, 80 mg.kg-1) and colchicine (0.20 mg.kg-1) ig, respectively. The rats were sacrificed 24 h after the last administration, serum and liver tissues were collected, the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the serum of rats were measured, and the activities of superoxide dismutase (SOD) ), Malondialdehyde (MDA), glutathione (GSH) and glutathione peroxidase (GSH-Px), and observed the pathological changes of liver tissue. Results: The serum levels of AST and ALT in each dose group of YLSF (20,40,80 mg.kg-1) were (207.85 ± 101.72), (131.55 ± 35.09), (129.98 ± 37.21) UL-1 and (90.51 The levels of SOD, MDA, GSH-Px and GSH in the liver tissue of YLSF groups were (143.14 ± 42.82), (146.53 ± 31.98 ± 4.44), (47.79 ± 16.11) and (44.56 ± 16.31) ), (147.41 ± 32.82) U.mg-1, (2.57 ± 0.54), (2.19 ± 0.57), (2.11 ± 0.59) nmol.mg-1, (463.55 ± 271.07), (659.14 ± 162.23) ± 200.70) nmol.mg-1, (5.06 ± 1.09), (6.10 ± 0.97), (6.89 ± 0.98) nmol.mg-1. The YLSF and the positive drugs at different dosages significantly reduced the levels of AST (P <0.01) and the content of MDA in liver tissue (P <0.05 or P <0.01), and significantly increased the content of SOD in liver tissue (P <0.05 or P <0.01 (P <0.01). The levels of GSH in the liver of rats were significantly increased (P <0.01). The middle and high doses of YLSF could significantly increase the level of ALT in rat serum GSH-Px (P <0.01). Each dose of YLSF and positive drug can reduce the degree of hepatocellular injury (P <0.05 or P <0.01). Conclusion: Yulangsan flavonoids have a certain therapeutic effect on CCl4-induced rats, and its mechanism may be related to its elimination of free radicals and inhibition of lipid peroxidation.