ACE2-Ang (1–7)/ SIRT1 is a Prospective Nephroprotective Panel of Dize in CCl4- Induced Kidney Injury. | ||
| Records of Pharmaceutical and Biomedical Sciences | ||
| Volume 9, Issue 1, March 2025, Pages 1-11 PDF (1.13 M) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/rpbs.2025.336171.1336 | ||
| Authors | ||
| El-Hassan Habib Mahmoud* 1; Dina Mohamed Abo elmaaty2; Sami Saleh3; Maivel H Ghattas4; Nesreen Nabil Omar5 | ||
| 1Major officer | ||
| 2Biochemistry, Pharmacy, Suez canal university, Ismalia, Egypt. | ||
| 3Biochemistry Depart., Faculty of Pharmacy Suez Canal University, Ismailia, Egypt | ||
| 4Medical Biochemistry Department, Faculty of Medicine, Port Said University | ||
| 5Department of Biochemistry, faculty of pharmacy,modern university for technology and information, Cairo, Egypt | ||
| Abstract | ||
| Carbon tetrachloride (CCl4) causes oxidative stress and inflammation in rats' kidneys, leading to renal damage. Mortality from renal damage is alarmingly rising, necessitating coordinated efforts to create a viable treatment. Renin-angiotensin system (RAS) modulation by angiotensin-converting enzyme 2 (ACE2 (is significant since the RAS is a key player in renal damage as a result of toxicity. Diminazene aceturate (DIZE), an ACE2 activator, has been shown to have positive benefits on models of renal disorders in earlier studies. In the current investigation, we sought to assess DIZE administration's therapeutic effects on rat experimental renal damage brought on by CCl4. Male Albino rats were treated with either CCl4 (0.5 mg/kg twice/week) and/or Dize (15 mg/kg/day) for eight weeks. In this study, CCl4 rats activated the RAS system as indicated by the downregulation of ACE2. The CCl4-induced inflammatory response was demonstrated through increased levels of TNF-α, IL-6, IFN-γ, and NF-κB and suppression of SIRT1. Conversely, Dize elicited protective action, upregulated the expression of ACE2, and suppressed the inflammation. In conclusion, Dize inhibited the RAS system and provided renoprotection while suppressing the proinflammatory response caused by CCl4. | ||
| Keywords | ||
| CCl4; Diminazene; SIRT1; ACE2; RAS | ||
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