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目的观察谷氨酰胺(Gln)对脂多糖(LPS)诱导的血管平滑肌细胞(vascular smooth muscle cells,VSMCs)异常增殖的影响。方法检测Gln对LPS作用下VSMCs的TLR4 mRNA及蛋白质表达,TNF-α、IL-10 mRNA表达及VSMCs增殖率,并进行相关性分析。结果应用LPS后VSMCs内的TLR4、TNF-α mRNA表达均增强,而IL-10 mRNA表达减弱(P<0.05,P<0.01)。应用Gln后,TLR4及TNF-α的mRNA表达[(0.926 9±0.108 2)及(1.021 4±0.190 1)]较单纯应用LPS[(0.965 0±0.146 3)及(1.369 8±0.290 4)]下降,而IL-10 mRNA表达由(0.228 9±0.049 1)增加至(0.468 9±0.109 9)。与LPS组相比,Gln干预后TNF-α与IL-10 mRNA变化差异均有统计学意义(P<0.05)。LPS可以诱导VSMCs内TLR4蛋白表达增高(P<0.01),Gln作用LPS诱导的VSMCs后,TLR4蛋白质表达下降,并显著低于LPS组,但仍明显高于对照组(P<0.01)。相关性分析显示,TLR4蛋白与TNF-α、IL-10 mRNA表达及VSMCs增殖的相关系数r分别为0.922 5、-0.867 4及0.989 2。结论谷氨酰胺可抑制LPS诱导的血管平滑肌细胞炎症反应及增殖,增加抗炎症反应,TLR4可能是这一作用机制的关键点。
Objective To investigate the effects of glutamine on the abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by lipopolysaccharide (LPS). Methods The expression of TLR4 mRNA and protein, the mRNA expression of TNF-α, IL-10 and the proliferation rate of VSMCs in VSMCs treated with Ln were measured by Gin and their correlations were analyzed. Results The expression of TLR4 and TNF-α mRNA in VSMCs increased and the expression of IL-10 mRNA decreased (P <0.05, P <0.01). The mRNA expression of TLR4 and TNF-α [(0.926 9 ± 0.108 2) vs (1.021 4 ± 0.190 1)] was significantly higher than that of LPS [(0.965 ± 0.146 3) and (1.369 8 ± 0.290 4) , While IL-10 mRNA expression increased from (0.228 9 ± 0.049 1) to (0.468 9 ± 0.109 9). Compared with LPS group, the difference of TNF-α and IL-10 mRNA expression after Gln intervention were statistically significant (P <0.05). LPS induced an increase in TLR4 protein expression in VSMCs (P <0.01). The TLR4 protein expression decreased after Gln administration of LPS-induced VSMCs, but was significantly lower than that in LPS group (P <0.01). Correlation analysis showed that the correlation coefficients between TLR4 protein and TNF-α, IL-10 mRNA and VSMCs proliferation were 0.922 5, -0.867 4 and 0.989 2, respectively. Conclusion Glutamine can inhibit the LPS-induced inflammatory response and proliferation of vascular smooth muscle cells and increase the anti-inflammatory response. TLR4 may be the key point of this mechanism.