Metabolic syndrome or syndrome X is the name given to the collection of clinical conditions including overweight, high blood pressure, high blood glucose (or type 2 diabetes mellitus), and hyperlipidemia (Chen et al., 2017).Metabolic syndrome is the most important risk factor for atherosclerosis in response to chronic inflammation and vascular endothelial dysfunction. Metabolic syndrome increases the risk of cardiovascular diseases. Cardiovascular diseases are the main reasons for mortality around the world . The metabolic syndrome is rising due to a sedentary lifestyle. Children, adolescents, and young women with polycystic ovary syndrome are at risk for metabolic syndrome (Vassallo et al., 2016).Medicine herbs, because of their potential efficacy in improving and holding human health, low cost, and adverse effects, have been the focus of attention. Studies have been shown that several plants and their active constituents can exert beneficial effects on metabolic syndrome. For example, grapes (Vitis vinifera), a source of polyphenol antioxidants, is useful for preventing the risk factors involved in metabolic syndromes such as hyperlipidemia, hypertension, and hyperglycemia (Akaberi & Hosseinzadeh, 2016). Garlic (Allium sativum) has been documented in the treatment of metabolic syndrome as it showed hypoglycemic, hypotensive, and hypolipidemic activities (Hosseini & Hosseinzadeh, 2015). Rosemary (Rosmarinus officinalis L.) is a source of phenolic phytochemicals having considerable anti-inflammatory, antioxidant, hypoglycemic, hypolipidemic, and hypotensive effects (Hassani et al., 2016).
Purpose: Rhabdomyolysis (RM) is a serious fatal syndrome. The RM leads to acute kidney injury (AKI) as a fatal complication. The belief is that the RM-induced AKI is triggered by myoglobin (MB). MB activates oxidative and apoptotic pathways.Trans-sodium crocetinate (TSC) isobtained from saffron and it has antioxidant andrenoprotective effects. This research was designed to assess the mechanisms of MB-induced cytotoxicity in HEK-2 cells (human embryonic kidney cells) as well as the possible effects of TSC against MB-induced cytotoxicity. Methods: HEK-2 cells were exposed to diverse concentrations of TSC (2.5, 5, 10, 20, 40, 80, and 100 µM) for 24 h. Then, MB (9 mg/ml) was added to the cells. After 24 h, cell viability was measured through MTT, and The values of ROS generation were calculated using DCFH-DA assay. Besides, using western blot autophagy and apoptosis markers in cells were assessed. Results: MB decreased viability and increased ROS levels in HEK-2 cells. Furthermore, MB enhanced the apoptosis markers (cleaved caspase-3 and Bax/Bcl-2 ratio) and autophagy markers (LC3II/I ratio and Beclin-1) in HEK-2 cells. However, pretreatment of HEK-2 cells with TSC for 24 h reduced the cytotoxicity and ROS production caused by MB. Additionally, TSC pretreatment condensed the levels of autophagy and apoptosis markers in response to MB cytotoxicity. Conclusion:TSC has a positive effect in preventing MB-induced cytotoxicity in HEK-2 cells by increasing antioxidant activity and regulation of apoptotic and autophagy signaling pathways.
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