Department of Neurology, Affiliated Hospital of Jiangnan University, Wuxi, 214000, Jiangsu, China.
Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi, 214000, Jiangsu, China.
Inflammation. 2020 Dec;43(6):2109-2118. doi: 10.1007/s10753-020-01278-x.
Panaxatriol saponins (PTS) have a long history in the treatment of stroke. In our previous experiments, PTS has been found to alleviate ischemic stroke and play a role through regulating the inflammatory response, but the specific mechanism of its regulation is still unclear. Cell viability was determined by MTT assay. Expressions of polarization-related proteins CD16, CD68, ARG1 and CD206; inflammatory factors interleukin-1β (IL-1β); inducible nitric oxide synthase (iNOS); monocyte chemotactic protein 1(MCP-1) and cyclooxygenase-2 (COX-2); apoptosis-related proteins pro-caspase3; bax; caspase3 and bcl-2; and STAT3 and p-STAT3 were detected by western blot. ELISA was used to detect the expression of inflammatory-related factors in cells. The apoptosis rate was detected by flow cytometry. We found that the survival rate of oxygen sugar deprivation/reoxygenation (OGD/R) cells increased obviously after PTS treatment in a dose-dependent manner. PTS can promote M2 polarization of microglial cells (BV2) and inhibit inflammatory response of OGD/R cells, accompanied by decreased expression of inflammatory factors IL-1β, iNOS, MCP-1, and COX-2. PTS inhibited apoptosis of OGD/R cells and was accompanied by decreased expression of apoptotic proteins Bax and caspase3 and increased expression of Bcl-2. We also found that PTS activated STAT3 levels in BV2 cells. After the addition of STAT3 inhibitor Stattic, it was found that PTS could promote M2 polarization of BV2 cells by activating the STAT3 pathway, thus inhibiting cell inflammation and apoptosis. PTS promoted M2 polarization in microglia cells by activating the STAT3 pathway, thereby reducing cell inflammation and apoptosis after glucose/oxygen deprivation.
人参三醇型皂苷（PTS）在治疗中风方面有着悠久的历史。在我们之前的实验中，已经发现 PTS 可以通过调节炎症反应来减轻缺血性中风，并发挥作用，但具体的调节机制仍不清楚。通过 MTT 法测定细胞活力。通过 Western blot 检测极化相关蛋白 CD16、CD68、ARG1 和 CD206；炎症因子白细胞介素-1β（IL-1β）；诱导型一氧化氮合酶（iNOS）；单核细胞趋化蛋白 1（MCP-1）和环氧化酶-2（COX-2）；凋亡相关蛋白 pro-caspase3；bax；caspase3 和 bcl-2；以及 STAT3 和 p-STAT3 的表达。ELISA 用于检测细胞中炎症相关因子的表达。通过流式细胞术检测细胞凋亡率。我们发现 PTS 处理后，氧糖剥夺/复氧（OGD/R）细胞的存活率明显增加，呈剂量依赖性。PTS 可促进小胶质细胞（BV2）M2 极化，抑制 OGD/R 细胞炎症反应，同时降低炎症因子 IL-1β、iNOS、MCP-1 和 COX-2 的表达。PTS 抑制 OGD/R 细胞凋亡，同时降低凋亡蛋白 Bax 和 caspase3 的表达，增加 Bcl-2 的表达。我们还发现 PTS 激活了 BV2 细胞中的 STAT3 水平。加入 STAT3 抑制剂 Stattic 后，发现 PTS 通过激活 STAT3 通路促进 BV2 细胞 M2 极化，从而抑制细胞炎症和凋亡。PTS 通过激活 STAT3 通路促进小胶质细胞 M2 极化，从而减少葡萄糖/氧剥夺后细胞炎症和凋亡。
