Background and Aims Hepatic ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical practice, which usually occurs in liver transplantation, liver resection, severe trauma, and hemorrhagic shock. Proanthocyanidin (PC), exerted from various plants with antioxidant, antitumor, and antiaging activity, were administrated in our study to investigate the underlying mechanism of its protective function on IRI. Methods Two doses of PC (50 mg/kg, 100 mg/kg) were given to BALB/c mice by intragastric administration for 7 days before partial (70%) warm IR surgery. Serum and liver tissues were collected 2, 8, and 24 h after reperfusion for relevant experiments. Results The results of transaminase and hematoxylin and eosin staining indicated that PC pretreatment significantly alleviated IRI in mice. Serum total superoxide dismutase increased and malondialdehyde decreased in PC pretreatment groups. Enzyme-linked immunosorbent assays, western blotting, quantitative real-time polymerase chain reaction, and immunohistochemistry showed that inflammation, apoptosis, and autophagy in PC preprocessing groups were significantly inhibited and were dose-dependent. The protein, mRNA expression, and immunohistochemical staining results of peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) in the PC pretreatment groups were significantly upregulated compared with the IR group in a dose-dependent manner. Conclusions PC pretreatment suppressed inflammation, apoptosis, and autophagy via the PPAR-α signaling pathway to protect against IRI of the liver in mice.

中文翻译：

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原花青素通过 PPARα/PGC1α 信号通路抑制自噬和细胞凋亡，从而减轻肝脏缺血/再灌注损伤。

背景与目的肝缺血再灌注损伤（IRI）是临床上常见的病理生理现象，多发生于肝移植、肝切除、严重创伤、失血性休克等情况。我们的研究中使用了从多种植物中提取的具有抗氧化、抗肿瘤和抗衰老活性的原花青素（PC），以探讨其对 IRI 保护功能的潜在机制。方法在部分（70%）温热IR手术前，给BALB/c小鼠灌胃2个剂量的PC（50 mg/kg、100 mg/kg），连续7 d。再灌注后2、8、24 h采集血清和肝组织用于相关实验。结果转氨酶和苏木精伊红染色结果表明PC预处理显着减轻小鼠IRI。PC预处理组血清总超氧化物歧化酶升高，丙二醛降低。酶联免疫吸附试验、蛋白质印迹、实时定量聚合酶链反应和免疫组织化学结果表明，PC预处理组的炎症、细胞凋亡和自噬受到显着抑制，且呈剂量依赖性。PC预处理组过氧化物酶体增殖物激活受体α（PPARα）和过氧化物酶体增殖物激活受体γ共激活物1-α（PGC1α）的蛋白、mRNA表达量和免疫组化染色结果与IR组相比在一定剂量下显着上调依赖方式。结论 PC预处理通过PPAR-α信号通路抑制炎症、细胞凋亡和自噬，从而预防小鼠肝脏IRI。