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目的:研究玉郎伞黄酮(YLSF)对四氯化碳(CCl4)所致小鼠急性化学性肝损伤的保护作用及机制。方法:将小鼠分为正常对照组(NC),模型对照组(MC),YLSF高(YLSFH)、YLSF中(YLSFM)、YLSF低(YLSFL)剂量组,及联苯双酯组(BPDC)。NC组及MC组以生理盐水ig,各剂量YLSF组和阳性对照组分别给予YLSF(112,56,28 mg.kg-1)和BPDC(150 mg.kg-1)ig,连续给药7 d,每天1次。以分光光度法测定各组小鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)活性、白蛋白(Alb)含量以及总抗氧化能力(T-AOC),以及肝组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,并于光镜观察小鼠肝损伤程度。结果:YLSF高、中剂量YLSF能降低血清AST、ALT、ALP含量(P<0.01)及肝组织MDA含量(P<0.01),增加血清Alb含量(P<0.01),提升血清T-AOC水平(P<0.01)及肝组织T-SOD活力(P<0.01);低剂量YLSF能降低血清AST、ALP含量(P<0.01或P<0.05)及肝组织MDA含量(P<0.01),增加血清Alb含量,但对小鼠血清ALT含量、血清T-AOC水平及肝组织T-SOD活力的影响无统计学意义。同时,各剂量YLSF均能减轻肝细胞损伤程度(P<0.01,P<0.05)。结论:YLSF对CCl4诱导的小鼠急性化学性肝损伤具有显著保护作用,其作用机制可能与其抗氧自由基抑制脂质过氧化作用有关。
Objective: To study the protective effect and mechanism of YLSF on acute chemical liver injury induced by carbon tetrachloride (CCl4) in mice. Methods: The mice were divided into normal control group (MC), model control group (MC), YLSFH, YLSFM, YLSFL low dose group and BPDC group, . The rats in NC group and MC group were given YLSF (112, 56, 28 mg.kg-1) and BPDC (150 mg.kg-1) ig respectively with physiological saline ig every dose YLSF group and positive control group, , 1 day. The serum levels of ALT, AST, ALP, Alb and total antioxidant capacity (T-test) were determined by spectrophotometry (T- AOC), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in liver tissue were observed. The degree of liver injury in mice was observed with light microscope. Results: YLSF at high and medium doses reduced serum AST, ALT and ALP contents (P <0.01) and liver MDA content (P <0.01), increased serum Alb levels (P <0.01) and elevated serum T-AOC levels (P <0.01) and the activity of T-SOD in liver tissue (P <0.01). Low dose of YLSF could decrease the level of AST and ALP (P <0.01 or P <0.05) But had no significant effect on serum ALT level, serum T-AOC level and liver T-SOD activity. At the same time, each dose of YLSF can reduce the degree of hepatocellular injury (P <0.01, P <0.05). CONCLUSION: YLSF has a significant protective effect on CCl4-induced acute chemical liver injury in mice, and its mechanism may be related to its inhibition of lipid peroxidation by antioxidant free radicals.