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马铃薯蛋白水解物和运动在预防快速老化小鼠高脂饮食诱导的肝细胞凋亡中的作用。

Role of potato protein hydrolysate and exercise in preventing high-fat diet-induced hepatocyte apoptosis in senescence-accelerated mouse.

机构信息

Department of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan, ROC.

HK. Zen Heart Group Biopharmaceutical Co. Limited, Wanchai, Hong Kong.

出版信息

J Food Biochem. 2020 Dec;44(12):e13525. doi: 10.1111/jfbc.13525. Epub 2020 Oct 19.

DOI:10.1111/jfbc.13525
PMID:33078424
Abstract

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. PRACTICAL APPLICATIONS: Exercise training is proven to reduce the health problems associated with aging and obesity, however, intensity and duration of the exercise differs between individuals. We used integrated pharmacological and nonpharmacological approach as a therapeutic strategy for preventing HFD-induced hepatic injury in aged subjects.

摘要

非酒精性脂肪性肝病(NAFLD)被认为是一种严重的临床并发症,可导致严重的肝功能障碍,包括纤维化、肝硬化和肝癌。肥胖可导致 NAFLD,并导致肝脏紊乱和相关的复杂肝脏疾病。本研究旨在探讨运动联合碱性蛋白酶处理衍生的马铃薯蛋白水解物(APPH)对快速老化小鼠品系 8(SAMP8)高脂饮食(HFD)诱导肝损伤的影响。将小鼠分为六组(n=6):第 I 组-对照组,第 II 组-HFD,第 III 组-运动,第 IV 组-HFD+APPH,第 V 组-HFD+运动,第 VI 组-HFD+运动+APPH。与 APPH 治疗和运动单独治疗相比,联合 APPH 治疗和运动对 HFD 诱导的组织学变化提供了更好的细胞保护作用。此外,APPH 和运动激活细胞存活蛋白 PI3K/Akt,并防止 FasL/FADD 介导的 HFD 喂养 SAMP8 小鼠中的细胞凋亡。游泳运动联合 APPH 可通过激活 PI3K/Akt 蛋白,有效调节 HFD 诱导的老年小鼠肝损伤和细胞凋亡。实际应用:运动训练已被证明可减少与衰老和肥胖相关的健康问题,但个体之间的运动强度和持续时间不同。我们使用综合的药理学和非药理学方法作为预防老年人群 HFD 诱导肝损伤的治疗策略。

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