首页|The Effect of Regulating miR-223 Expression on the Expression of Inflammatory Factors and Renal Interstitial Fibrosis in a Rat Model of Chronic Glomerulonephritis and its Relationship with the IL-6/STAT3 Signaling Pathway
The Effect of Regulating miR-223 Expression on the Expression of Inflammatory Factors and Renal Interstitial Fibrosis in a Rat Model of Chronic Glomerulonephritis and its Relationship with the IL-6/STAT3 Signaling Pathway
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Objective:To explore the effect of miR-223 on the expression of in-flammatory factors and renal interstitial fibrosis in a rat model of chronic glomeru-lonephritis based on the interleukin 6/signal transducer and activator of transcription 3 (IL-6/STAT3) signaling pathway. Methods:A total of 70 SPF-grade healthy adult male SD rats were selected,and were randomly divided into five groups. Except for the blank group,the remaining four groups of rats were all subcutaneously injected with 1 mg/mL cationized bovine serum albumin (C-BSA) emulsion at multiple points (in the first week) and injected with 2.5 mg/mL C-BSA solution through the tail vein (from the 2nd to 4th week) to establish a glomerulonephritis model. After successful modeling,the blank group and the modeling group were injected with normal saline through the tail vein,the negative control group was injected with 50 μg/kg NC agomir through the tail vein,the miR-223 agonist group was injected with 50 μg/kg miR-223 agomir through the tail vein,and the pathway activation group was injected with 50 μg/kg miR-223 agomir and 1 μg/kg rhIL-6 through the tail vein. After continuous treatment for 21 d,the rats were sacrificed and kidney tissues were taken. The expression of miR-223,in-flammatory factors and IL-6/STAT3 signaling pathway-related proteins in the five groups of rats was observed and compared,and the renal interstitial fibrosis in the five groups of rats was also observed and compared. Results:The relative expression level of miR-223 in the blank group was significantly higher than that in the other four groups. The relative expression levels of miR-223 in the miR-223 agonist group and the pathway activation group were significantly higher than those in the model group and the negative control group (P<0.05). The expression levels of IL-1β,IL-17,TNF-α,and TGF-β1 in the blank group were lower than those in the other four groups. The expression levels of IL-1β,IL-17,TNF-α,and TGF-β1 in the model group and the negative control group were significantly higher than those in the miR-223 agonist group and the pathway activation group. The expression levels of IL-1β,IL-17,TNF-α,and TGF-β1 in the pathway activation group were higher than those in the miR-223 agonist group (P<0.05). The proportion of renal interstitial fibrosis area in renal tissue of the blank group was significantly lower than that in the other four groups. The propor-tion of renal interstitial fibrosis area in renal tissue of the model group and the negative control group was higher than that in the miR-223 agonist group and the pathway acti-vation group. The proportion of renal interstitial fibrosis area in renal tissue of the pathway activation group was higher than that in the miR-223 agonist group (P<0.05). The expression levels of IL-6/GAPDH and p-STAT3/STAT3 in the blank group were lower than those in the other four groups. The expression levels of IL-6/GAPDH and p-STAT3/STAT3 in the model group and the negative control group were significantly higher than those in the miR-223 agonist group and the pathway activation group. The expression levels of IL-6/GAPDH and p-STAT3/STAT3 in the pathway activation group were higher than those in the miR-223 agonist group (P<0.05). Conclusion:The ex-pression of inflammatory factors and renal interstitial fibrosis in rats with chronic glomerulonephritis are affected by miR-223. The mechanism may be related to the ex-pression of IL-6/STAT3 signaling pathway-related proteins.
NETL
NSTL
万方数据
