Related Experiment Video
Updated: Sep 20, 2026
Rapid Quantification of Mitogen-induced Blastogenesis in T Lymphocytes for Identifying Immunomodulatory Drugs
Published on: December 27, 2016
[Effect of triamcinolone acetonide on the proliferation and monocyte chemoattractant protein expression in rat
Xiao-chuan Wu1, Zhu-wen Yi, Jian-wu Xiao
1Laboratory of Pediatric Nephrology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Objective:
To explore the inhibitory effect and mechanism of triamcinolone acetonide (TA) on the proliferation and monocyte chemoattractant protein-1(MCP-1) expression in rat glomerular mesangial cells (GMCs).
Methods:
TA with different concentrations was put in the cultured rat GMC line in vitro after Lipopolysaccharide (LPS). There were three groups in our experiment: the GMC group, LPS group (GMCs + LPS), and TA group(GMCs + LPS + TA). The GMC proliferation level was detected by the 3-(4,5-Dimethylthiazol-2-yl)2,5-diphenyltetrazo-lium bromid (MTT) incorporation at the 24th and 48th hours. The expression of MCP-1 and nuclear transcriptional factor-Kappa B (NF-kappa B) were checked by immunohistochemistry. The MCP-1 concentration was determined by ELISA.
Results:
1. In the TA group, the GMC proliferative level was obviously lower than that either in the LPS group or in the GMC group (P < 0.01). 2. The MCP-1 expression of GMCs in the TA group was obviously lower than that in any of the other groups (P < 0.01). 3. The NF-kappa B expression in GMCs in the TA group was significantly lower than that in the LPS group (P < 0.01), but there was no significant difference in the NF-kappa B expression between the TA group and LPS group (P > 0.05). 4. The concentration of MCP-1 in the TA group was obviously lower than that in the LPS group (P < 0.01), while there was no significant difference in the MCP-1 concentration between the TA group and the GMC group (P > 0.05).
Conclusion:
TA can obviously inhibit the proliferation of GMCs, and down-regulate the abnormal expression and secretion of MCP-1 by reducing the activation of NF-kappa B.
