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Berberine ameliorates cellular senescence and extends the lifespan of mice via regulating p16 and cyclin protein expression

机译:小檗碱改善细胞衰老,并通过调节p16和细胞周期蛋白表达延伸小鼠的寿命

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Although aging and senescence have been extensively studied in the past few decades, however, there is lack of clinical treatment available for anti‐aging. This study presents the effects of berberine (BBR) on the aging process resulting in a promising extension of lifespan in model organisms. BBR extended the replicative lifespan, improved the morphology, and boosted rejuvenation markers of replicative senescence in human fetal lung diploid fibroblasts (2BS and WI38). BBR also rescued senescent cells with late population doubling (PD). Furthermore, the senescence‐associated β‐galactosidase (SA‐β‐gal)‐positive cell rates of late PD cells grown in the BBR‐containing medium were ~72% lower than those of control cells, and its morphology resembled that of young cells. Mechanistically, BBR improved cell growth and proliferation by promoting entry of cell cycles from the G 0 or G 1 phase to S/G 2 ‐M phase. Most importantly, BBR extended the lifespan of chemotherapy‐treated mice and naturally aged mice by ~52% and ~16.49%, respectively. The residual lifespan of the naturally aged mice was extended by 80%, from 85.5?days to 154?days. The oral administration of BBR in mice resulted in significantly improved health span, fur density, and behavioral activity. Therefore, BBR may be an ideal candidate for the development of an anti‐aging medicine.
机译:虽然在过去的几十年中,老化和衰老已经过广泛研究,但缺乏可用于抗衰老的临床治疗。本研究提出了Berberine(BBR)对老化过程的影响,导致模型生物中的寿命延伸。 BBR扩展了复制的寿命,改善了人体胎儿肺二倍体成纤维细胞(2BS和Wi38)的复制衰老的形态学和促进了复合标记。 BBR还拯救了晚期群体加倍(PD)的衰老细胞。此外,在含BBR培养基中生长的晚期PD细胞的衰老相关的β-半乳糖苷酶(SA-β-GAL) - 阳性PD细胞的阳性细胞率低于对照细胞的72%,其形态类似于幼细胞的形态。机械地,BBR通过从G 0或G 1相进入S / G 2 -M相,通过促进细胞循环的进入来改善细胞生长和增殖。最重要的是,BBR分别将化疗处理的小鼠的寿命扩展,天然老化的小鼠分别〜52%和〜16.49%。天然老年小鼠的残余寿命延长80%,从85.5?天到154.天。小鼠中BBR的口服给药导致了有显着改善的健康跨度,毛皮密度和行为活动。因此,BBR可以是开发抗衰老医学的理想候选者。

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