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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.

Author information

1
Department of Graduate School, Tianjin Medical University, Tianjin, 300051, China.
2
Department of Radiology, The Second Affiliated Hospital of Baotou Medical College, Baotou, 014030, Neimenggu, China.
3
Department of General Surgery, The First Affiliated Hospital of USTC, Hefei, 230001, Anhui, China.
4
Department of General Surgery, The First Affiliated Hospital of USTC, Hefei, 230001, Anhui, China. xugeliang2019@sina.com.
5
Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
6
Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt.

Abstract

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.

KEYWORDS:

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

PMID:
31863371
DOI:
10.1007/s11356-019-07117-3

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