Nonalcoholic fatty liver disease (NAFLD) is considered to be a serious clinical complication, which could cause significant liver dysfunction including fibrosis, cirrhosis, and cancer. Obesity could lead to NAFLD and contributes to liver disorder and related complicated liver diseases. Effect of exercise combined with alcalase treatment derived potato protein hydrolysate (APPH) on high‐fat diet (HFD)‐induced hepatic injury was investigated in senescence accelerated mouse‐prone 8 (SAMP8) mice in the present study. Mice were divided into six groups (n = 6): Group I‐Control, Group II‐HFD, Group III‐Exercise, Group IV‐HFD + APPH, Group V‐HFD + Exercise, and Group VI‐HFD + Exercise + APPH. Combined APPH treatment and exercise offer better cytoprotection in HFD‐induced histological changes than APPH treatment and exercise alone. Further, APPH and exercise activate the cell survival proteins PI3K/Akt and prevent FasL/FADD‐mediated apoptosis in HFD fed SAMP8 mouse. APPH with swimming exercise effectively modulate HFD‐induced liver damage and apoptosis in aged mice through activation of PI3K/Akt protein.

中文翻译：

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马铃薯蛋白水解物和运动在防止高脂饮食诱导的衰老加速小鼠肝细胞凋亡中的作用

非酒精性脂肪肝疾病（NAFLD）被认为是一种严重的临床并发症，可能引起严重的肝功能障碍，包括纤维化，肝硬化和癌症。肥胖可能导致NAFLD，并导致肝脏疾病和相关的复杂肝脏疾病。在本研究中，研究了运动与碱性蛋白酶处理衍生的马铃薯蛋白水解产物（APPH）结合对高脂饮食（HFD）诱导的肝损伤的影响。将小鼠分为六组（n = 6）：第I组-对照组，第II组-HFD，第III组-锻炼，第IV-HFD + APPH，第V-HFD +锻炼，第VI-HFD +锻炼+ APPH。与仅APPH治疗和运动相比，APPH治疗和运动相结合在HFD诱导的组织学改变中提供了更好的细胞保护。此外，APPH和运动激活了HFD喂养的SAMP8小鼠的细胞存活蛋白PI3K / Akt，并阻止了FasL / FADD介导的细胞凋亡。游泳运动的APPH通过激活PI3K / Akt蛋白有效调节衰老小鼠的HFD诱导的肝损伤和细胞凋亡。