Curcumin phytosome modulates aluminum-induced hepatotoxicity via regulation of antioxidant, Bcl-2, and caspase-3 in rats
- PDF / 824,422 Bytes
- 9 Pages / 595.276 x 790.866 pts Page_size
- 86 Downloads / 179 Views
RESEARCH ARTICLE
Curcumin phytosome modulates aluminum-induced hepatotoxicity via regulation of antioxidant, Bcl-2, and caspase-3 in rats Mohammed Al-Kahtani 1 & Mohamed M. Abdel-Daim 2,3 & Amany A. Sayed 4 & Attalla El-Kott 1,5 & Kareem Morsy 1,4 Received: 10 August 2019 / Accepted: 27 March 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Increasing entrance of aluminum chloride (AlCl3) in many fields exposes human beings to its biotoxicity. Thereby, the present study assesses the potential ameliorative role of curcumin phytosome (CP) on AlCl3-induced hepatotoxicity. Rats were divided into four groups (n = 6): group 1 served as control; group 2 received CP (200 mg CP/kg b.wt) for 21 days; group 3 injected three doses of AlCl3 (30 mg/kg/body weight) every 5 days intraperitoneally; group 4 received CP for 7 days prior to AlCl3 and then received CP concurrently with AlCl3 for another 14 days. AlCl3 markedly increased (P < 0.05) the concentrations of AST, ALT, ALP, LDH, total bilirubin, and LPO as well as depleted (P < 0.05) albumin, GSH, SOD, and GPx stores in comparison to the control group. These biochemical alterations supported by the lesion observed in histological sections, increasing the expression of caspase-3 and decreasing the expression of Bcl-2. Treatment with CP modulates the hepatic dysfunction, boosting the endogenous antioxidant status, downregulating the expression of caspase-3, and upregulating the expression of Bcl-2. This hepatic ameliorative effect may be mediated by the ability of CP to repair the oxidant/antioxidant equilibrium rather than its ability to suppress apoptosis. Keywords Hepatotoxicity . Curcumin phytosome . Antioxidants . Apoptosis
Introduction Aluminum (Al) is the third most abundant element in the earth’s crust. Its extensive consumption especially in the newly daily life style and its entrance in industrial products expose human beings to potential risks (Taïr et al. 2016). The prolonged exposure of aluminum chloride (AlCl3) provokes hepatic toxicity due to its detoxification function (Hasona and Ahmed 2017). Responsible editor: Philippe Garrigues * Amany A. Sayed [email protected] 1
Department of Biology, College of Science, King Khalid University, Abha, Saudi Arabia
2
Department of Zoology, Science College, King Saud University, Riyadh 11451, Saudi Arabia
3
Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia 41522, Egypt
4
Department of Zoology, Faculty of Science, Cairo University, Cairo, Egypt
5
Department of Zoology, Faculty of Science, Damanhour University, Damanhour, Egypt
AlCl3 disturbs the oxidative/antioxidative balance, as it enhances lipid peroxidation (LPO) and diminishes the activities of the antioxidant enzymes consequently generating oxidative stress (OxS), causing toxicity (Hasona and Ahmed 2017; Zahedi-Amiri et al. 2018). Further, AlCl3 dysregulates apoptosis via stimulation of the pro-oxidant properties of iron and copper resulting in deterioration of mitochondrial dysfunction
Data Loading...
