竹节参总皂苷对高脂高糖小鼠脑组织凋亡的保护作用

Protective Effect of Saponins from Panax japonicus on Brain Apoptosis in Mice with High-fat and High-fructose Diet

摘要:

观察竹节参总皂苷（saponins from Panax japonicas，SPJ）对高脂高糖饮食小鼠脑组织凋亡的保护作用。昆明小鼠随机分成正常对照组、高脂高糖模型组和药物低（100 mg/kg）、高（300 mg/kg）剂量组，分别给予普通饲料、高脂高糖饲料、竹节参总皂苷低、高剂量饲料喂养。Western blot法检测抑凋亡相关蛋白Bcl-2、促凋亡蛋白Bax、细胞色素C（Cytochrome C）、半胱天冬蛋白酶（Caspase-3和Caspase-12）、炎性因子诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS）、环氧合酶2（cyclooxygenase，COX-2）、IL-1β和NLRP3炎症小体包括NOD样受体家族3（NOD-like receptors，NLRP3）、凋亡相关斑点样蛋白（ASC）、Caspase-1和抗氧化应激蛋白沉默信息调节因子1（Silence information regulator 1，SIRT1）、腺苷酸活化蛋白激酶（Adenosine monophosphate activated protein kinase，AMPK）磷酸化水平。与高脂对照组相比，竹节参总皂苷高剂量组中Bcl-2、SIRT1和p-AMPK分别升高了1.31倍、1.05倍、1.33倍，Bax、Caspase 3、Caspase 12、Cytochrome C、COX-2、iNOS、IL-1β、NLRP3、Caspase 1和ASC分别下降了34%、39%、60%、37%、41%、25%、43%、49%、31%、52%。竹节参总皂苷对高脂高糖小鼠具有抗凋亡作用，其机制与其调节NLRP3炎症小体及炎性因子，增加抗氧化应激相关蛋白有关。

Abstract:

The objective in this work was to investigate the effect of saponins from Panax japonicus (SPJ) on high-fat and high-fructose diet (HFFD) induced apoptosis in mice. KM mice were divided into normal control, high-fat and high-fructose-diet group, low-dose SPJ group (100 mg/kg) and high-dose SPJ group (300 mg/kg) and were fed with normal diet, high-fat and high-fructose diet (HFFD) and HFFD followed by SPJ at different doses (100 and 300 mg/kg) for one month, respectively. The protein levels of Bcl-2, Bax, Cytochrome C, Caspase-3, Caspase-12, COX-2, iNOS, IL-1β, NLRP3, Caspase-1, ASC, SIRT1 and p-AMPK were detected by western blot. The results showed that the protein levels of Bcl-2, SIRT1 and p-AMPK of high-dose SPJ group increased by 1.31, 1.05 and 1.33 times, respectively. The protein levels of Bax、Caspase 3、Caspase 12、Cytochrome C、COX-2、iNOS、IL-1β、NLRP3、Caspase 1 and ASC decreased by 34%、39%、60%、37%、41%、25%、43%、49%、31%、52%, respectively. In conclusion, SPJ have strong anti-apoptosis effect on mice with high-fat and high-fructose diet, and its mechanism is related with inhibition of NLRP3 inflammasome activitation, resulting in a reduction of expression of inflammatory factors, or the upregulation of the proteins associated with oxidative stress.