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Environ Sci Pollut Res Int. 2019 Dec 20. doi: 10.1007/s11356-019-07117-3. [Epub ahead of print]

Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats.

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Department of Graduate School, Tianjin Medical University, Tianjin, 300051, China.
Department of Radiology, The Second Affiliated Hospital of Baotou Medical College, Baotou, 014030, Neimenggu, China.
Department of General Surgery, The First Affiliated Hospital of USTC, Hefei, 230001, Anhui, China.
Department of General Surgery, The First Affiliated Hospital of USTC, Hefei, 230001, Anhui, China.
Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt.


Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride (CdCl2)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), CdCl2 (0.6 mg/kg), and SAE + CdCl2, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before CdCl2 exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by CdCl2 exposure. SAE can be used as a promising protective agent against CdCl2-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract.


Apoptosis; Cadmium; Inflammation; Liver; Nuclear factor erythroid 2-related factor 2; Oxidative stress; Senna alexandrina


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