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| The knockout of nuclear factor E2 related factor and its effect on myofibroblast activation and renal fibrosis |
| CHENG Shuibing1, GUO Yangyang2, ZHU Hengyue2, XIAO Yanyi2, ZHENG Shizhang2, QI Ruyi2, ZHOU Junlei2, YANG Mei3, BAI Yongheng2 |
| 1.Department of Trauma Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 3.Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China |
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| Cite this article: |
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CHENG Shuibing,GUO Yangyang,ZHU Hengyue, et al. The knockout of nuclear factor E2 related factor and its effect on myofibroblast activation and renal fibrosis[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(4): 300-305，311.
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Abstract Objective: To investigate the knockout of nuclear factor E2 related factor (Nrf2) and its effect on the activation of renal myofibroblasts and interstitial fibrosis. Methods: Mice were randomly divided into four groups: Nrf2-wild-type sham group, Nrf2-knock-out sham group, Nrf2-wild-type unilateral ureteral obstruction (UUO) group and Nrf2-knock-out UUO group, with 6 mice in each group. The levels of serum creatinine and urea nitrogen were determined by biochemical analyzer; Periodic acid-Schiff staining (PAS) was used to observe the degree of renal damage; Masson staining was used to evaluate the accumulation of total collagen in renal interstitium; immunohistochemical staining was used to analyze the expression levels of myofibroblastic marker α-SMA, matrix component type III collagen and transforming growth factor β1 (TGF-β1); qRT-PCR was used to detect the mRNA expression of TGF-β1. Results: Compared with the Nrf2-wild-type sham group, the serum creatinine and urea nitrogen levels in the Nrf2-wild-type UUO group were significantly increased (P<0.05). There was no significant difference in serum creatinine and urea nitrogen levels between the Nrf2-wild-type UUO group and the Nrf2-knock-out UUO group (P>0.05). PAS staining showed that renal tissue damage was significantly aggravated in the Nrf2-knock-out UUO group (P<0.01), compared with the Nrf2-wild-type UUO group; Masson staining showed that total accumulation of renal interstitial collagen in the Nrf2-knock-out UUO group was significantly increased (P<0.01), compared with the Nrf2-wild-type UUO group; immunohistochemical staining showed that the expression of α-SMA and type III collagen in renal tissue of Nrf2-knock-out UUO group was significantly increased (P<0.05), compared with the Nrf2-wild-type UUO group, which was related to TGF-β1 mRNA and protein expression caused by Nrf2 knockout (P<0.05). Conclusion: Nrf2 knockout can aggravate the degree of renal injury and fibrosis caused by ureteral obstruction. Its mechanism may be related to Nrf2 knockout that increases TGF-β1 levels, resulting in excessive activation of myofibroblasts and collagen accumulation in renal interstitium.
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