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马铃薯蛋白水解物中的生物活性二肽与游泳运动相结合,通过激活 SAMP8 小鼠中的 PI3K/Akt,预防高脂饮食诱导的肝细胞凋亡。

Bioactive dipeptide from potato protein hydrolysate combined with swimming exercise prevents high fat diet induced hepatocyte apoptosis by activating PI3K/Akt in SAMP8 mouse.

机构信息

Department of Emergency Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan.

Department of Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan.

出版信息

Mol Biol Rep. 2021 Mar;48(3):2629-2637. doi: 10.1007/s11033-021-06317-w. Epub 2021 Mar 31.

DOI:10.1007/s11033-021-06317-w
PMID:33791907
Abstract

Obesity in aged population have surges the occurrence of various metabolic disorders including Nonalcoholic fatty liver disease (NAFLD). Apoptosis in the liver is one of the causative factors for NAFLD-induced liver damage. Plants derived bioactive peptides have been shown as an alternative treatment approach for the treating NAFLD due to its less toxicity. Moderate exercise has been reported to improve cellular physiological function prevent age associated metabolic disorders. In the present study, we evaluate the effects of bioactive dipeptide (IF) derived from alcalase potato-protein hydrolysates and swimming exercise in preventing High Fat Diet (HFD)-induced liver damage in senescence accelerated mouse-prone 8 (SAMP8) mice model. Mouse were fed with HFD for 6 weeks followed by oral IF administration or swimming exercise and both for 8 weeks. HFD induces significant structural changes in liver of HFD fed SAMP8 mouse. Both IF administration and exercise prevent the structural abnormalities induced by HFD, however, combined IF treatment and exercise offer better protection. Combined IF treatment and exercise activate PI3K/Akt cell survival protein and effectively inhibit Fas-FADD-induced apoptosis in HFD fed aged mouse. Oral supplementation of bioactive peptide IF combined with moderate swimming exercise effectively alleviate HFD-induced hepatic injury in aged mice.

摘要

肥胖在老年人群中激增,导致各种代谢紊乱,包括非酒精性脂肪性肝病(NAFLD)。肝脏细胞凋亡是导致 NAFLD 肝损伤的原因之一。植物来源的生物活性肽因其毒性较小,已被证明是治疗 NAFLD 的一种替代治疗方法。适度运动已被报道可改善细胞生理功能,预防与年龄相关的代谢紊乱。在本研究中,我们评估了来源于碱性蛋白酶马铃薯蛋白水解物的生物活性二肽(IF)以及游泳运动对加速老化敏感 8 号小鼠(SAMP8)模型高脂饮食(HFD)诱导的肝损伤的预防作用。小鼠用 HFD 喂养 6 周,随后进行 IF 口服给药或游泳运动,均持续 8 周。HFD 诱导 HFD 喂养的 SAMP8 小鼠的肝脏结构发生显著变化。IF 给药和运动均可预防 HFD 引起的结构异常,但联合 IF 治疗和运动提供更好的保护。联合 IF 治疗和运动激活了 PI3K/Akt 细胞存活蛋白,并有效抑制了 HFD 喂养的老年小鼠中 Fas-FADD 诱导的细胞凋亡。口服补充生物活性肽 IF 联合适度游泳运动可有效减轻老年小鼠的 HFD 诱导的肝损伤。

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