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Abstract: TH-PO935

Silence of Central (Pro)renin Receptor Ameliorates Salt-Induced Renal Injury and Oxidative Stress in CKD

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms


  • Li, Jiawen, Nanfang Hospital, Southern Medical University, Guangzhou, GUangDong, China
  • Zhang, Mengbi, Nanfang Hospital, Southern Medical University, Guangzhou, GUangDong, China
  • Tan, Lishan, Nanfang Hospital, Southern Medical University, Guangzhou, GUangDong, China
  • Qiu, Minzi, Nanfang Hospital, Southern Medical University, Guangzhou, GUangDong, China
  • Li, Aiqing, Nanfang Hospital, Southern Medical University, Guangzhou, GUangDong, China

High salt diet promotes renal injury and oxidative stress via the brain and renal RAS axis in CKD rats. (Pro)renin receptor(PRR) can mediate oxidative stress. However, central PRR regulates salt-induced renal oxidative stress in CKD remains undefined. Here we hypothesized that the reduction of central PRR expression could ameliorate oxidative stress and thereby prevent renal injury in high-salt-load CKD rats.


We used the lentivirus as a vector to screen out the sequences that inhibit the central PRR expression in mature rat hippocampal neural stem cells in vitro.Moreover, we investigated renal oxidative stress, renin-angiotensin system, sympathetic nerve activity and tissue injury in 5/6 nephrectomy CKD model rats fed high dietary salt after silence of central PRR expression by intracerebroventricular (ICV) lentivirus RNAi.


We found that high salt diet contributes to progression of renal injury, fibrosis and oxidative stress in CKD; The expression of PRR in the subfornical organ was decreased after ICV administration of lentivirus RNAi, indicating that shRNA successfully inhibited the expression of PRR in the brain. The expression of tyrosine hydroxylase in neurons of the rostral ventrolateral medulla of the brain, and the serum, renal norepinephrine levels were decreased, indicating that activation of the sympathetic nerve system was prevented by silence of central PRR expression; while kidney H&E staining and Sirius Red staining, as well as Fibronectin, α-SMA, and Collagen I were down-regulated, indicating that inhibition of central PRR can improve renal injury and reduce renal fibrosis. In addition, renal RAS components such as PRR, Angiotensinogen, and Angiotensin II, and kidney NADPH oxidase (Nox2, Nox4) were down-regulated, while renal antioxidant enzymes (CAT, GP1, and SOD1) were up-regulated. These experimental data suggest that silencing PRR expression in the CNS may down-regulate renal RAS expression and reduce renal damage and oxidative stress levels.


Silence of central PRR expression ameliorates renal fibrosis, injury, and oxidative stress in CKD model fed high salt.