Article ID Journal Published Year Pages File Type
2583329 Environmental Toxicology and Pharmacology 2013 14 Pages PDF
Abstract

Salvianic acid A (SAA) is the main hydrophilic active ingredient of Salvia miltiorrhiza bunge, which has long been used to treat liver and heart disease in China. In the present study, we investigated the radioprotective effects of SAA against γ-radiation-induced apoptosis in cultured human embryo liver L-02 cells. The results demonstrated that SAA markedly inhibited γ-radiation induced apoptosis, decreased DNA damage, and increased the intracellular antioxidative ability of the L-02 cells. SAA exhibited radioprotection by decreasing the generation of reactive oxygen species, inhibiting the release of mitochondrial cytochrome C, blocking the activation of caspase-3, and down regulating the expression of Bax and P53 and up regulating the expression of Bcl-2. This indicated that SAA pretreatment inhibited the caspase-dependent mitochondria apoptosis pathway. The radioprotection of the SAA pretreatment was also evidenced by an increased survival ratio, maintaining the antioxidant enzyme levels in the liver, inhibition of oxidative stress, and relative low liver and renal toxicity compared with estriol exposure. In conclusion, SAA may be an effective radioprotector against γ-radiation induced apoptosis in L-02 cells and damage in mice, the antioxidant potency of SAA might be correlated with the beneficial radioprotectant effects observed.

► Salvianic acid A (SAA) has long been used for treating liver and heart diseases in China. ► SAA can significantly inhibit γ-radiation induced apoptosis and DNA damage in L-02 cells. ► SAA can protect the balance of the pro-oxidant and antioxidant in the cells and prevent the generation of ROS induced by γ-radiation. ► SAA exhibited radioprotection by inhibiting the release of mitochondrial Cyt c and activation of caspase-3 and regulating the expressions of apoptosis related proteins.

Related Topics
Life Sciences Environmental Science Health, Toxicology and Mutagenesis
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