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Panax notoginseng saponins promote liver regeneration through activation of the PI3K/AKT/mTOR cell proliferation pathway and upregulation of the AKT/Bad cell survival pathway in mice

机译:Panax Noginseng Saponins通过激活PI3K / AKT / MTOR细胞增殖途径来促进肝脏再生,并在小鼠中的AKT /坏细胞存活途径的上调

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摘要

Abstract Backgroud The regenerative capacity of the liver is crucial for the host to survive after serious hepatic injuries, tumor resection, or living donor liver transplantation. Panax notoginseng saponins (PNS) have been reported to exert protective effects during organ injuries. The present study aimed to evaluate the effect of PNS on liver regeneration(LR) and on injuries induced by partial hepatectomy (PH). Methods We performed 70% partial PH on C57BL/6 J mice treated with or without PNS. LR was estimated by liver weight/body weight, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and cell proliferation, and the related cellular signals were analyzed by Western blot. Results Different concentrations of PNS promoted hepatocyte proliferation in vitro. Mice in the PNS group showed higher liver/body weight ratios at 2 d and 7 d (P < 0.05) after PH and lower levels of serum ALT and AST (P < 0.05) compared to those of mice in the normal control (NC) group. Histological analysis showed that the expression of proliferating cell nuclear antigen(PCNA) at 2 d and 7 d after PH was significantly higher in the PNS group than in the NC group (P < 0.05). Mechanistically, the AKT/mTOR cell proliferation pathway and AKT/Bad cell survival pathway were activated by PNS, which accelerated hepatocyte proliferation and inhibited apoptosis (P < 0.05). Conclusions PNS promoted liver regeneration through activation of PI3K/AKT/mTOR and upregulated the AKT/Bad cell pathways in mice.
机译:摘要研究背景肝脏的再生能力是至关重要的主机严重的肝损伤,肿瘤切除,或活体肝移植术后存活。三七总皂苷(PNS)已报告中发挥脏器损伤的保护作用。本研究的目的是评估对肝再生(LR)和由部分肝切除(PH)诱导的损伤PNS的效果。方法我们对C57BL进行70%的部分PH有或没有处理过的PNS / 6 J小鼠。 LR通过肝脏重量/体重,血清谷丙转氨酶(ALT)和天冬氨酸转氨酶(AST)的水平和细胞增殖估计,以及相关的细胞信号通过蛋白质印迹进行分析。结果不同浓度的PNS的体外促进肝细胞增殖。小鼠PNS组在术后2 d和7 d(P <0.05)显示出较高的肝/体重比相比于正常对照的那些小鼠的PH和血清ALT和AST水平较低(P <0.05)(NC)团体。组织学分析表明,PH后2 d和7 d增殖细胞核抗原(PCNA)的表达显著越高PNS组比NC组(P <0.05)英寸机械地,所述AKT / mTOR的细胞增殖途径和AKT /坏细胞存活途径被PNS,这加速肝细胞增殖和抑制凋亡(P <0.05)被激活。结论PNS通过PI3K / AKT / mTOR的激活促进肝脏再生和小鼠上调AKT /坏细胞途径。

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