Dissertation
Dissertation > Medicine, health > Surgery > Urology ( urinary and reproductive system diseases) > Kidney disease > Nephritis

Effects of Inflammatory Factors on Proliferation of Human Mesangial Cells and Protective Effects of Troglitazone

Author LiuLinYan
Tutor LiQiu
School Chongqing Medical University
Course Pediatrics
Keywords Troglitazone Mesangial cells Tumor necrosis factor - alpha Nuclear factor - kappa B Intercellular adhesion molecule-1
CLC R692.3
Type Master's thesis
Year 2008
Downloads 29
Quotes 0
Download Dissertation

Objective: To observe the troglitazone induced apoptosis in human tumor necrosis factor alpha (TNF-alpha) mesangial cells (HMCL) proliferation and cell adhesion molecule -1 (ICAM-1) mRNA and protein expression, and to explore troglitazone role in the inflammation-induced mesangial cells and its possible mechanism for the clinical treatment of pharmacological targets and theoretical basis. Methods: Cultured HMCL divided into control group, different concentrations of TNF-alpha induced group, different concentrations of troglitazone intervention group, troglitazone control group. MTT assay (MTT) to detect the level of cell proliferation, reverse transcription - polymerase chain reaction (RT-PCR) assay in each group mesangial cell ICAM-1 mRNA expression levels, enzyme-linked immunosorbent assay (ELISA ) to detect the mesangial cell culture supernatant ICAM-1 protein expression levels, immunocytochemistry (ICC) was detected in each group mesangial cells NF-kappa B protein expression levels. Results: (1) The results of the MTT method: different concentrations of TNF-alpha group mesangial cell proliferation was significantly higher than the control group (P lt; 0.05), showing a peak of proliferation in the TNF-alpha-induced 48h, 24h, and There were significant differences (P lt; 0.05) 6h group, various concentrations of troglitazone intervention group mesangial cell proliferation was significantly lower than the level of TNF-alpha-induced group (P lt; 0.05). (2) RT-PCR results: different concentrations of TNF-alpha induced group ICAM-1 mRNA expression was significantly higher compared with the control group, a statistically significant difference (P lt; 0.05), and various concentrations of troglitazone intervention group mesangial cells ICAM-1 mRNA expression was significantly lower than TNF-alpha induced group (P lt; 0.05). (3) ELISA analysis: different concentrations of TNF-alpha induced ICAM-1 protein expression was significantly increased compared with the control group, a statistically significant difference (P lt; 0.05), various concentrations of troglitazone ketone intervention group mesangial cell ICAM 1 protein expression was significantly lower than TNF-alpha-induced group (P lt; 0.05) (4) ICC analysis: different concentrations of TNF-alpha induced group NF-kappa B protein expression was significantly increased compared with the control group, a statistically significant difference (P lt; 0.05), various concentrations of troglitazone the ketone intervention group mesangial cell NF-kappa B protein expression was significantly lower than TNF-alpha-induced group (P lt; 0.05). Conclusion: (1) TNF-alpha can enhance the proliferation of mesangial cells, increase cell surface ICAM-1 mRNA and protein expression of the NF-kappa B protein expression increased, suggesting that TNF-alpha can promote increased mesangial cell inflammatory response. (2) troglitazone can reduce TNF-alpha-induced mesangial cell proliferation and reduced TNF-alpha-induced cell surface ICAM-1 mRNA and protein expression increased, suggesting that troglitazone can inhibit TNF-alpha induced mesangial cells in the inflammatory response. (3) troglitazone can reduce the expression of TNF-alpha-induced mesangial cell NF-kappa B protein, suggesting that troglitazone may reduce TNF-alpha induced by inhibiting NF-kappaB signal transduction pathway in mesangial cells ICAM-1 the expression.

Related Dissertations
More Dissertations