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目的:研究石斛多糖(DP)对环孢素A(CsA)诱导的肝损伤的防治作用并探讨其作用机制。方法:将Wistar雄性大鼠随机分为6组:①正常对照组:单纯胃饲橄榄油;②CsA组:CsA溶解于橄榄油,按CsA50mg.kg-1.d-1胃饲;③DP组:胃饲DP50mg.kg-1.d-1和相同体积的橄榄油;④CsA+低DP组:CsA50mg.kg-1.d-1和DP10mg.kg-1.d-1;⑤CsA+中DP组:CsA50mg.kg-1.d-1和DP50mg.kg-1.d-1;⑥CsA+高DP组:CsA50mg.kg-1.d-1和DP250mg.kg-1.d-1,实验连续21d。21d后测定大鼠血清中总胆红素(TBIL)、丙氨酸转氨酶(ALT)、天门冬氨酸氨基转移酶(AST)、白蛋白(ALB)及肝组织匀浆甘油三酯(TRIG)、丙二醛(MDA)、还原性谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和ATPase(超微量分型),并作肝组织病理学检测。结果:DP能缓解CsA诱导的大鼠血清TBIL、AST、ALT含量的增加和ALB含量的降低,DP减轻CsA所致的大鼠肝匀浆中的MDA、TRIG的升高和GSH、SOD、Na+,K+-ATPase、Ca2+-ATPase、Mg2+-ATPase的损耗(P<0.05或P<0.01),减轻CsA肝毒性所致肝组织变性、坏死程度等病理改变。结论:DP对CsA所致的大鼠肝损伤具有防治作用,其作用机制可能与DP的抗脂质过氧化作用和抑制细胞氧化磷酸化的解耦联有关。
Objective: To study the preventive and therapeutic effects of Dendrobium nobile polysaccharide (DP) on cyclosporine A (CsA)-induced liver injury and to explore its mechanism of action. Methods: Wistar male rats were randomly divided into 6 groups: 1 normal control group: stomach fed with olive oil; 2CsA group: CsA dissolved in olive oil, CsA 50mg.kg-1.d-1 stomach feeding; 3DP group: stomach Feeding DP50mg.kg-1.d-1 and the same volume of olive oil; 4CsA+low DP group: CsA50mg.kg-1.d-1 and DP10mg.kg-1.d-1; 5CsA+ DP group: CsA50mg.kg -1.d-1 and DP50mg.kg-1.d-1; 6CsA+high DP group: CsA50mg.kg-1.d-1 and DP250mg.kg-1.d-1 for 21 days. After 21 days, serum total bilirubin (TBIL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB) and liver homogenate triglyceride (TRIG) were measured. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), and ATPase (ultramicrotyping) were used for liver histopathological examination. Results: DP alleviated the increase of serum TBIL, AST, ALT and ALB content in rats induced by CsA. DP reduced the increase of MDA and TRIG in rat liver homogenate and GSH, SOD, Na+ induced by CsA. The loss of K+-ATPase, Ca2+-ATPase and Mg2+-ATPase (P<0.05 or P<0.01) decreased the pathological changes of hepatic tissue degeneration and necrosis caused by CsA hepatotoxicity. Conclusion: DP has preventive and therapeutic effects on CsA-induced hepatic injury in rats, and its mechanism may be related to the anti-lipid peroxidation of DP and the decoupling of inhibition of cellular oxidative phosphorylation.