Hepatoprotective Assessment of Copper Calx against Anti-Tubercular Drug-induced Hepatotoxicity in Rats

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Abstract
Pharmacognosy Research,2023,15,4,806-812.
Published:October 2023
Type:Original Article
Authors:
Author(s) affiliations:

Mohammad Sharique1, Hariprasad M.G1,2,*, Moqbel Ali Moqbel Redhwan1,2, Ashish Jain1, Shambhavi S1, Mamatha A3, Niranjana4

1Department of Pharmacology, KLE College of Pharmacy, Bengaluru, Karnataka, INDIA.

2Basic Science Research Center (Off-Campus), KLE College of Pharmacy, Bengaluru, Karnataka, INDIA.

3Department of Pharmacognosy, KLE College of Pharmacy, Bengaluru, Karnataka, INDIA. 4Pentacare Ayur Pharma, Malleshwaram, Bengaluru, Karnataka, INDIA.

Abstract:

Background: Anti-Tubercular Drugs (ATDs), while effective in treating tuberculosis, are associated with hepatotoxicity, leading to liver damage and complications. Calx of Copper, a traditional Ayurvedic preparation, has shown potential hepatoprotective properties. Objectives: To investigate the potential hepatoprotective role of Calx of Copper in mitigating ATD-induced hepatotoxicity and to examine its impact on liver function markers and histopathological changes in rats. Materials and Methods: Thirty male Wistar rats were randomly divided into five groups (n=6 per group): control, ATD, Calx of Copper, ATD+Calx of Copper, and silymarin (used as a standard hepatoprotective agent). Hepatotoxicity was induced in the ATD, ATD+Calx of Copper, and silymarin groups by administering a combination of isoniazid, rifampicin, and pyrazinamide for 25 days. Calx of Copper and silymarin were orally administered at doses of 6.17 mg/kg and 12.33 mg/kg, and 300 mg/kg b.w, respectively, in their respective groups. Liver function markers, including serum transaminase and alanine Aminotransferase (ALT), were measured at the end of the study. A histopathological examination of liver tissues was also performed. Results: ATDinduced hepatotoxicity was evident through elevated serum SGPT, SGOT, ALT, and ALP levels and histopathological alterations in liver tissue. Co-administration of Calx of Copper significantly reduced SGPT, SGOT, ALT, and ALP (p<0.05) and improved liver histopathological changes compared to the ATD group. The hepatoprotective effect of Calx of Copper was comparable to that of silymarin. Conclusion: Copper calx demonstrated significant hepatoprotective activity against ATD-induced hepatotoxicity in rats, as evidenced by normalizing liver function markers and histopathological improvements. These findings suggest that Calx of Copper may be a promising adjuvant therapy for mitigating liver damage associated with anti-tubercular drug treatment.

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Effect of Calx of Copper against antitubercular drugs (INH, RIF, and PYZ) induced histopathological alteration in experimental groups of rats (H&E staining @ 40X). (A) Normal control, (B) positive control anti- tubercular drugs (INH, RIF, and PYZ) induced rat liver damage, (C and D) Histological Examination of Hepatic Tissue in Rats Administered with Copper Calx at Doses of 6.17 mg/kg and 12.33 mg/kg, (E) Histological Analysis of Hepatic Tissue in Silymarin-Treated Rats.

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