Haifeng Yang, Xiaolan Chen, Yanyan Li, Jing Wang, Feifei Shi, Bin Li, Yiyi Hu
{"title":"青藤碱对lps刺激内皮细胞ERK1/2、JNK和p38磷酸化的影响。","authors":"Haifeng Yang, Xiaolan Chen, Yanyan Li, Jing Wang, Feifei Shi, Bin Li, Yiyi Hu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>This study was to investigate the effect of sinomenine by LPS-induced MAPK phosphorylation in endothelial cells. Endothelial cells were challenged with different doses LPS and/or treated with sinomenine at three concentrations (1, 5, or 10 μg/mL) in pathological model, drug safety, treatment and prevention experiments. The cells were incubated at 37 °C in a cell incubator total for 24 h. The lysate cells were collected and analyzed the phosphorylation of ERK1/2, JNK and p38 by MAPK phosphoprotein assay whole cell lysate kit. As expected, LPS could significantly elevated phosphorylation of ERK1/2, JNK and p38, but sinomenine not. The results revealed that sinomenine significantly reduced the phosphorylation of ERK1/2 and p38 in treatment experiment, and inhibited phosphorylation of ERK1/2, JNK and p38 in prevention experiment. Our findings demonstrated that sinomenine protects endothelial cells from LPS-induced inflammation, which might be associated with depressing MAPK signaling pathway.</p>","PeriodicalId":0,"journal":{"name":"","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The effect of sinomenine on ERK1/2, JNK and p38 phosphorylation in LPS-stimulated endothelial cells.\",\"authors\":\"Haifeng Yang, Xiaolan Chen, Yanyan Li, Jing Wang, Feifei Shi, Bin Li, Yiyi Hu\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>This study was to investigate the effect of sinomenine by LPS-induced MAPK phosphorylation in endothelial cells. Endothelial cells were challenged with different doses LPS and/or treated with sinomenine at three concentrations (1, 5, or 10 μg/mL) in pathological model, drug safety, treatment and prevention experiments. The cells were incubated at 37 °C in a cell incubator total for 24 h. The lysate cells were collected and analyzed the phosphorylation of ERK1/2, JNK and p38 by MAPK phosphoprotein assay whole cell lysate kit. As expected, LPS could significantly elevated phosphorylation of ERK1/2, JNK and p38, but sinomenine not. The results revealed that sinomenine significantly reduced the phosphorylation of ERK1/2 and p38 in treatment experiment, and inhibited phosphorylation of ERK1/2, JNK and p38 in prevention experiment. Our findings demonstrated that sinomenine protects endothelial cells from LPS-induced inflammation, which might be associated with depressing MAPK signaling pathway.</p>\",\"PeriodicalId\":0,\"journal\":{\"name\":\"\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0,\"publicationDate\":\"2023-03-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"","FirstCategoryId":"3","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The effect of sinomenine on ERK1/2, JNK and p38 phosphorylation in LPS-stimulated endothelial cells.
This study was to investigate the effect of sinomenine by LPS-induced MAPK phosphorylation in endothelial cells. Endothelial cells were challenged with different doses LPS and/or treated with sinomenine at three concentrations (1, 5, or 10 μg/mL) in pathological model, drug safety, treatment and prevention experiments. The cells were incubated at 37 °C in a cell incubator total for 24 h. The lysate cells were collected and analyzed the phosphorylation of ERK1/2, JNK and p38 by MAPK phosphoprotein assay whole cell lysate kit. As expected, LPS could significantly elevated phosphorylation of ERK1/2, JNK and p38, but sinomenine not. The results revealed that sinomenine significantly reduced the phosphorylation of ERK1/2 and p38 in treatment experiment, and inhibited phosphorylation of ERK1/2, JNK and p38 in prevention experiment. Our findings demonstrated that sinomenine protects endothelial cells from LPS-induced inflammation, which might be associated with depressing MAPK signaling pathway.