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| Effects of Qufeng Tongluo Fomula on the inflammatory responce of human glomerular mesangial cells induced by high glucose |
| SU Guanxun1 LI Lina2 CHEN Yu1 ZHAO Boxu1 ZHANG Yaofu1 ZHAO Jinxi1 HUANG Weijun1 WANG Shidong1 |
1.The Second Department of Endocrinology and Nephropathy, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100010, China;
2.School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China |
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Abstract Objective To investigate the effects of Qufeng Tongluo Fomula on the inflammatory responce of human mesangial cells induced by high glucose. Methods In vitro culture of human mesangial cells, they were divided into normal group (low-glucose DMEM culture medium + normal rat serum), model group (high-glucose DMEM culture medium + normal rat serum), inhibitor group (high-glucose DMEM culture medium + normal rat serum +5 μmol/L SB203580 pretreatment), Qufeng Tongluo group (high-glucose DMEM culture medium + serum of rat taking Qufeng Tongluo Fomula). The levels of interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1) were detected by enzyme-linked immunosorbent assay. Western blot was used to detect the expression levels of p38 mitogen activation protein kinase (p38 MAPK), intercelluar adhesion molecule-1 (ICAM-1), and monocyte chemotactic protein-1 (MCP-1). The mRNA expressions of IL-1β, IL-6, TNF-α, TGF-β1, ICAM-1, MCP-1, and p38 MAPK were determined by RT-PCR. Results The levels and mRNA expression of IL-1β, IL-6, TNF-α, TGF-β1, ICAM-1, MCP-1, and p38 MAPK in model group were higher than those in normal group, the differences were statistically significant (P ＜ 0.05). The levels of IL-1β, IL-6, TNF-α, TGF-β1, ICAM-1, MCP-1, and p38 MAPK and their mRNA expression in Qufeng Tongluo group were lower than those in model group, and the differences were statistically significant (P ＜ 0.05). Conclusion Qufeng Tongluo Formula may reduce the expression of inflammatory factors in human glomerular mesangial cells induced by high glucose by inhibiting the p38 MAPK signaling pathway, thus alleviating the inflammatory response.
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