tannins and Acute-Kidney-Injury

Mercury (Hg) causes severe nephrotoxicity in subjects with excess exposure. This work attempted to identify whether a natural medicine--rhubarb--has protective effects against mercuric chloride (HgCl₂)-induced acute renal failure (ARF), and which of its components contributed most to the treatment. Total rhubarb extract (TR) were separated to the total anthraquinones (TA), the total tannins (TT) and remaining component extract (RC). Each extract was orally pre-administered to rats for five successive days followed by HgCl₂ injection to induce kidney injury. Subsequently, renal histopathology and biochemical examinations were performed in vitro to evaluate the protective effects. Pharmacological studies showed that TR and TA, but not TT or RC manifested significant protection activity against HgCl₂-induced ARF. There were also significant declines of serum creatine, urea nitrogen values and increases of total protein albumin levels in TR and TA treated groups compared to HgCl₂ alone (p < 0.05). At last, the major components in TA extract were further identified as anthraquinones by liquid chromatography coupled mass spectroscopy. This study thus provides observational evidences that rhubarb could ameliorate HgCl₂-induced ARF and its anthraquinones in particular are the effective components responsible for this activity in rhubarb extract.

Topics: Acute Kidney Injury; Animals; Anthraquinones; Humans; Mercuric Chloride; Plant Extracts; Protective Agents; Rats; Rheum; Tannins

Cisplatin (CP) is a well-known chemotherapeutic drug that displays dose-limiting nephrotoxicity. In this study, tannic acid (TA), a naturally occurring plant polyphenol, was evaluated for its antioxidant and antigenotoxicity potential against the CP-induced renal oxidative stress and genotoxicity in Swiss albino mice. The mice were given a prophylactic treatment of TA orally at a dose of 40 and 80 mg/kg body weight (b wt) for 7 consecutive days before the administration of a single intraperitoneal (i.p.) injection of CP at 7 mg/kg b wt. The modulatory effects of TA on CP-induced nephrotoxicity and genotoxicity were investigated by assaying oxidative stress biomarkers, serum kidney toxicity markers, DNA fragmentation, alkaline unwinding, micronuclei assay, and by histopathological examination of kidney architecture. CP administration altered the antioxidant levels, enhanced lipid peroxidation, induced DNA strand breaks, and altered the levels of micronuclei among polychromatic erythrocytes (PCEs) significantly (p < 0.001). Pretreatment of TA in mice showed significant (p < 0.001) recovery in antioxidant status, viz., reduced glutathione content and its dependent enzymes, quinone reductase and γ-glutamyl transpeptidase. TA significantly (p < 0.001) reinstated the normal serum levels of blood urea nitrogen (BUN) and creatinine. TA showed strongly inhibited (p < 0.001) micronuclei induction, DNA strand breaks, and DNA fragmentation. Thus, TA as a phytochemical protects kidneys through its antigenotoxic activity and antioxidant potential.

Topics: Acute Kidney Injury; Animals; Antineoplastic Agents; Blood Urea Nitrogen; Cisplatin; Creatinine; DNA Damage; Glucosephosphate Dehydrogenase; Glutathione; Glutathione Reductase; Glutathione Transferase; Lipid Peroxidation; Male; Mice; Micronuclei, Chromosome-Defective; Protective Agents; Tannins; Xanthine Oxidase