Tricin Ameliorates Renal Fibrosis and Inhibits the Progression of Chronic Kidney Disease in Adenine-Induced Rats

Indian Journal of Pharmaceutical Education and Research

  • Yang Xu1Department of Nephrology, Affiliated Hospital of Hebei University; Key Laboratory of Bone Metabolism Physiology for Chronic Kidney Disease of Hebei Province, Baoding City, Hebei Province, CHINA.
  • Jianmin Zhang1Department of Nephrology, Affiliated Hospital of Hebei University; Key Laboratory of Bone Metabolism Physiology for Chronic Kidney Disease of Hebei Province, Baoding City, Hebei Province, CHINA.
  • Yapu Zhang1Department of Nephrology, Affiliated Hospital of Hebei University; Key Laboratory of Bone Metabolism Physiology for Chronic Kidney Disease of Hebei Province, Baoding City, Hebei Province, CHINA.
  • Yanli Gou1Department of Nephrology, Affiliated Hospital of Hebei University; Key Laboratory of Bone Metabolism Physiology for Chronic Kidney Disease of Hebei Province, Baoding City, Hebei Province, CHINA.
  • Qian Wang1Department of Nephrology, Affiliated Hospital of Hebei University; Key Laboratory of Bone Metabolism Physiology for Chronic Kidney Disease of Hebei Province, Baoding City, Hebei Province, CHINA.
  • Xuezhong Li2Department of Critical Care Medicine, Affiliated Hospital of Hebei University, Baoding City, Hebei Province, CHINA.
  • Kai Li3Department of Urology, Affiliated Hospital of Hebei University, Baoding City, Hebei Province, CHINA.

Volume 60 Issue 4 Pages 1587-1595

DOI: 10.5530/ijper.20263001

Abstract

Background: Renal fibrosis, a defining feature of Chronic Kidney Disease (CKD) development, is marked by the over deposition of extracellular matrix proteins, resulting in structural and functional impairment of the kidney. The limitations of existing therapies, together the escalating prevalence of CKD, highlight the pressing need for innovative therapeutic strategies that might proficiently avert or reverse renal fibrosis and maintain kidney functionality. Objectives: This study aimed to assess the impacts of tricin in a renal fibrosis induced by adenine in rats and to clarify the underlying pharmacological mechanisms of tricin. Materials and Methods: Renal fibrosis was induced in the experimental rats by administering 250 mg/kg of adenine daily for first two weeks, followed by every alternative day during the subsequent four weeks. Tricin at 50 and 100 mg/kg concentrations were administered to the rats daily from 2nd and 6th weeks. The body weights of the experimental rats were evaluated carefully on the weekly basis. Following the completion of the treatments, the levels of serum creatinine, Blood Urea Nitrogen (BUN), monophosphate levels, and inflammatory cytokine levels were evaluated. The kidneys of the experimental rats were subjected to histopathological analysis. Results: The treatment of tricin at 50 and 100 mg/kg concentrations markedly elevated body weight and subsequently reduced renal index in adenine-induced rats. Moreover, tricin treatment decreased the serum creatinine and BUN levels in the adenine-induced rats. Tricin treatment markedly reduced inflammatory cytokine levels and regulated the monophosphate levels in rats with renal fibrosis. The histological analysis confirmed the therapeutic effectiveness of tricin against the renal fibrosis. Conclusion: This study demonstrated that tricin ameliorated adenine-induced renal fibrosis and inhibited the progression of CKD in rats, which may be due to its anti-inflammatory properties.

Keywords

  • Creatinine
  • Inflammatory cytokines
  • Monophosphates
  • Renal fibrosis
  • Tricin
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