Tetrahydrocurcumin Potentially Attenuates Arsenic Induced Oxidative Hepatic Dysfunction in Rats

doi:10.4172/2161-0495.1000168

Cited by 5 publications

(3 citation statements)

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“…The activities of AST and ALT are sensitive indices of hepatic injury. Numerous studies have reported that elevated activities of AST and ALT in the plasma of arsenic-exposed rats are mainly attributed to cellular leakage and loss of functional integrity of hepatic membrane architecture [28,29]. Consistent with previous studies, we observed significantly higher levels of AST and ALT in rats exposed to arsenic than in control rats, probably resulting from hepatocyte membrane damage due to arsenic intoxication.…”

Section: Discussionsupporting

confidence: 91%

Biochanin A Ameliorates Arsenic-Induced Hepato- and Hematotoxicity in Rats

Jalaludeen

Lee

et al. 2016

Molecules

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Biochanin A (BCA) is a natural organic compound of the phytoestrogenic isoflavone class that has antioxidant and metal chelator properties in the presence of transition metal ions, however, its efficacy in animal models is still obscure. Therefore, the objective of this study was to investigate the protective effects of BCA against arsenic-induced hepatic injury and hematotoxicity in rats. The results suggest that arsenic intoxicated rats showed significantly higher levels of plasma hepatic markers than normal control rats. Furthermore, an increase in lipid peroxidation with depletion of reduced glutathione (GSH) and activities of superoxide dismutase (SOD) and catalase (CAT) occurred in the livers of rats exposed to arsenic. Administration of BCA (20 mg/kg¨bw/day) and selenium (3 mg/kg¨bw/day) resulted in a significant reversal of hepatic and oxidative stress markers in arsenic-intoxicated rats. A low dose of BCA (10 mg/kg¨bw/day) did not show any preventive effect, while a high dose of BCA (40 mg/kg¨bw/day) partially prevented all hepatotoxicity events. These biochemical perturbations were supported by histopathological observations of the liver. Our results suggest that administration of BCA (20 mg/kg¨bw/day) attenuated the arsenic hepatotoxicity, a property that could contribute to the therapeutic approaches for chronic liver diseases.

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Section: Discussionsupporting

confidence: 91%

Biochanin A Ameliorates Arsenic-Induced Hepato- and Hematotoxicity in Rats

Jalaludeen

Lee

et al. 2016

Molecules

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“…In vivo studies demonstrated the potential protective effect of THC against chloroquine- and arsenic-induced hepatotoxicity [ 25 , 26 ]. The efficacy of THC on metabolic dysfunction was tested in streptozotocin-induced type 2 diabetic rats, decreasing levels of plasma insulin and gluconeogenic enzymes and improving blood glucose and hepatic carbohydrate metabolism [ 27 , 28 ].…”

Section: Introductionmentioning

confidence: 99%

Tetrahydrocurcumin ameliorates free fatty acid-induced hepatic steatosis and improves insulin resistance in HepG2 cells

Chen

Kong

Tsai

et al. 2018

Journal of Food and Drug Analysis

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Elevated levels of free fatty acids (FFAs) in the liver, resulting from either increased lipolysis or imbalanced FFAs flux, is a key pathogenic factor of hepatic steatosis. This study was conducted to examine the therapeutic effect of tetrahydrocurcumin (THC), a naturally occurring curcuminoid and a metabolite of curcumin, on oleic acid (OA)-induced steatosis in human hepatocellular carcinoma cells and to elucidate the underlying mechanism. HepG2 cells were incubated with OA to induce steatosis, and then treated with various concentrations of THC. The results showed that THC treatment significantly decreased lipid accumulation in OA-treated HepG2 cells, possibly, by inhibiting the expression of the lipogenic proteins, sterol regulatory element-binding protein 1 (SREBP-1c), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), and fatty acid-binding protein 4 (FABP4). Moreover, THC attenuated OA-induced hepatic lipogenesis in an adenosine monophosphate-activated protein kinase (AMPK)-dependent manner, which was reversed by pretreatment with an AMPK inhibitor. THC promoted lipolysis and upregulated the expression of genes involved in β-oxidation. Glucose uptake and insulin signaling impaired in HepG2 cells incubated with OA were abated by THC treatment, including phosphorylation of the insulin receptor substrate 1 (IRS-1)/phosphoinositide 3-kinase (PI3K)/Akt and downstream signaling pathways, forkhead box protein O1 (FOXO1) and glycogen synthase kinase 3 β (GSK3β), which are involved in gluconeogenesis and glycogen synthesis, respectively. Altogether, these results demonstrated the novel therapeutic benefit of THC against hepatic steatosis and, consequently, a potential treatment for non-alcoholic fatty liver disease (NAFLD).

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“…This supports the observations reported 28,29 both As and Cd decreased body weight gain and food utilization and that these effects were more pronounced for the mixture. Available reports 30,31,32 also indicate that long term exposure to arsenic and cadmium could lead to significant reduction in body weights.…”

Section: Namentioning

confidence: 99%

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2018

IJPSR

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Cadmium (Cd) is a toxic heavy metal in the environment. The aim of this study was to investigate the potential effect of Cd on cholinergic and bioenergetic systems in three brain regions: cerebral cortex, cerebellum and hippocampus. The young albino rats (3 months) were exposed to low dose of Cd (1.5 mg/kg body weight) and high dose of Cd (3 mg/kg body weight) through intraperitoneal injection daily for a period of 3 weeks. A separate batch of rats were given α-tocopherol at a dose for a period of one week along with low and high dose of Cd. In this study, we observed that the AChE activity and ACh content in synaptosomal fractions and Mg 2+ -ATPase and Na + /K + -ATPase activities in mitochondrial fractions. We found the decrease in AChE, Mg 2+ -ATPase and Na + /K + -ATPase activities and increase in ACh content compared to control. The high dose of Cd treated rats showed maximal decrease in the AChE, Mg 2+ -ATPase and Na + /K + -ATPase activities and ACh content compared to low dose of Cd treated rats. The maximal alterations of these enzymes observed in hippocampus among three brain regions. Whereas, the rats supplemented with α-tocopherol along with Cd showed reversal effect with gradual increase in enzyme activities and decrease in ACh content. In addition to this, we found decrease in body weights in dose dependent manner upon Cd exposure. The above findings suggest Cd toxicity was reversed with α-tocopherol co-administration which could thus be considered for future applications as a neuroprotective agent against chronic exposure to Cd.

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Tetrahydrocurcumin Potentially Attenuates Arsenic Induced Oxidative Hepatic Dysfunction in Rats

Cited by 5 publications

References 61 publications

Biochanin A Ameliorates Arsenic-Induced Hepato- and Hematotoxicity in Rats

Biochanin A Ameliorates Arsenic-Induced Hepato- and Hematotoxicity in Rats

Tetrahydrocurcumin ameliorates free fatty acid-induced hepatic steatosis and improves insulin resistance in HepG2 cells

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