竹节参总皂苷通过激活自噬抑制衰老大鼠心肌细胞凋亡

Inhibition of Cardiomyocyte Apoptosis in Aging Rats by Saponins of Panax japonicus via Activating Autophagy

摘要:

观察竹节参总皂苷（total saponins of Panax japonica，TSPJ）对自然衰老大鼠心肌细胞凋亡的保护作用，并从自噬角度探讨其作用机制。取18月龄SD雄性大鼠随机分为模型组、TSPJ低、高剂量组，每组10只；TSPJ低、高剂量组分别投食给予TSPJ 10、30 mg/kg，模型组每天投食等量正常饲料，持续给药至24月龄；同时取10只6月龄大鼠作为对照组。与青年对照组相比，自然衰老组心肌细胞排列紊乱，肌纤维断裂，心肌细胞凋亡指数增加3倍。TSPJ能有效改善衰老大鼠心脏组织的形态结构和心肌细胞凋亡下降55%；衰老模型组Bax、Caspase-3、Caspase-9、p62蛋白表达分别升高了9.5，1.8，4.1，3.4倍，Bcl-2、Bcl-2/Bax及、LC3Ⅱ/ LC3Ⅰ、Beclin1分别下降了98%，99%，70%，48%；TSPJ组中Bax，Caspase-3，Caspase-9和p62分别下调87%、65%，70%和65%，Bcl-2，Bcl-2/Bax比值，LC3Ⅱ/LC3Ⅰ和Beclin1表达分别升高了12.75，138.5，5.68和2.6倍。结果表明，竹节参总皂苷能有效地改善衰老大鼠心肌细胞凋亡，其作用机制可能与TSPJ激活衰老大鼠心肌细胞自噬相关。

Abstract:

The protective effects of total saponins extracted from Panax japonicus (TSPJ) on cardiomyocyte apoptosis in natural aging rats, as well as its underlying mechanism in terms of autophagy was investigated. Male SD rats aged 18 months were randomly divided into 3 groups (model group, low-dose TSPJ group and high-dose TSPJ group), 10 rats in each group. TSPJ groups were given TSPJ at different doses (10 and 30 mg/kg, p.o.), model group was treated with equal normal animal food for 6 months until 24 months old. Another 10 rats aged 6 month (6M) were used controlled group. Compared to young control group, the myocardial cells arranged in disorder, and the muscle fibers broke, and cardiomyocyte apoptosis increased by 3 times in the natural aging group. TSPJ significantly improved the morphology of heart tissue and decreased cardiomyocyte apoptosis by 55% in comparison with natural aging group. Protein expression levels of Bax, Caspase-3, Caspase-9 and p62were increased by 9.5, 1.8, 4.1 and 3.4 times, the protein expression levels of Bcl-2, Bcl-2/Bax, LC3Ⅱ/ LC3Ⅰand Beclin1 was deceaesed by 98%, 99%, 70% and 48% in the aging group. TSPJ can effectively inhibit the protein expression of Bax, Caspase-3, Caspase-9 and p62 by 87%, 65%, 70% and 65%, and increase the expression of Bcl-2, Bcl-2 /Bax, LC3Ⅱ/ LC3Ⅰand Beclin1 by 12.75, 138.5, 5.68 and 2.6 times in the natural aging heart tissues. The results suggest that TSPJ can effectively improve cardiomyocyte apoptosis in natural aging rats, and its mechanism may be related to regulation of autophagy.