Ameliorative effect of camel's milk and Nigella Sativa Oil against thioacetamide-induced hepatorenal damage in rats

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Abstract
Pharmacognosy Magazine,2018,14,53,27-35.
Published:February 2018
Type:Original Article
Authors:
Author(s) affiliations:

Aftab Ahmad1, Fahad A Al-Abbasi2, Saida Sadath2, Soad Shaker Ali3, Mohammed F Abuzinadah4, Hani A Alhadrami4, Anwar Ali Mohammad Alghamdi1, Ali H Aseeri5, Shah Alam Khan6, Asif Husain7
1 Department of Health Information Technology, Jeddah Community College, King Abdulaziz University, Jeddah 21589, Saudi Arabia
2 Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah 21589, Saudi Arabia
3 Department of Anatomy, Faculty of Medicine, King Abdulaziz University, Scientific Chair of Yousef Abdullatif Jameel of Prophetic Medicine Application, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia
4 Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Saudi Arabia
5 Jeddah Regional Lab, Ministry of Health, Jeddah, Kingdom of Saudi Arabia
6 Department of Pharmacy, Oman Medical College, Muscat, Sultanate of Oman
7 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Hamdard University, New Delhi, India

Abstract:

Background: Camel milk (CM) and Nigella sativa (NS) have been traditionally claimed to cure wide range of diseases and used as medicine in different part of world, particularly in Saudi Arabia. Several research studies have been published that proved beneficial effects of CM and NS. Objective: This study was undertaken to investigate the antihepatotxic potential of CM and NS oil (NSO) against thioacetamide (TAA)-induced hepato and nephrotoxicity in rats. Materials and Methods: Thirty female Albino Wistar rats were randomly divided in to six groups having five rats in each group. A single subcutaneous injection of TAA (100 mg/kg b. w.) was administered to all the rats in Group-II to VI on 1st day to induce hepatorenal damage. Group I served as a normal control while Group II served as toxic control for comparison purpose. Experimental animals in Group III, IV, and V were supplemented with fresh CM, (250 mL/24 h/cage), NSO (2 mL/kg/day p. o.), and NSO + fresh CM, respectively. Group VI was treated with a polyherbal hepatoprotective Unani medicine Jigreen (2 mL/kg/day p. o.) for 21 days. TAA-induced hepatorenal damage and protective effects of CM and NSO were assessed by analyzing liver and kidney function tests in the serum. Histopathology of liver and kidney tissues was also carried out to corroborate the findings of biochemical investigation. Results: The results indicated that the TAA intoxicated rats showed significant increase in the alanine transaminase, aspartate transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase, lipid profile, urea, creatinine, uric acid, sodium, and potassium levels in serum. Treatment of rats with CM, NSO, and CM plus NSO combination and Jigreen significantly reversed the damage and brought down the serum biochemical parameters and lipid profile toward the normal levels. The histopathological studies also support the hepato and nephroprotective effects of CM and NSO. Conclusion: This study demonstrated the ameliorative effects of CM, NSO, and CM plus NSO combination against TAA-induced hepatorenal toxicity in rats.

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