Resveratrol (Res) has attracted great interest regarding its effects related to metabolic syndrome, especially for lipid metabolic disorder or insulin resistance; however, the underlying mechanisms remain elusive. To explore the effects of Res on insulin sensitivity and the underlying mechanism, insulin-resistant KKA(y) mice were treated with 2 and 4 g/kg diets of Res for 12 weeks. After the treatment, blood glucose, serum insulin, glucose tolerance, and insulin tolerance, as well as other indices such as adiponectin mRNA in epididymal adipose tissues, silent information regulator 1 (Sirt1), AMP-activated protein kinase (AMPK), insulin receptor substrate 1 (IRS1), and phosphorylated protein kinase B (PKB/AKT) proteins in liver and soleus muscles, were investigated. The results indicate that Res intervention reduces blood glucose and serum insulin levels, improves insulin and glucose tolerance, increases serum adiponectin and adiponectin mRNA levels in epididymal adipose tissues, and more importantly, elevates Sirt1, p-AMPK, p-IRS1, and p-AKT levels in liver and soleus muscles. In conclusion, Res could improve insulin sensitivity and ameliorate insulin resistance in KKA(y) mice, which may be associated with the upregulation of Sirt1 protein in liver and soleus muscles and consequent AMPK activation, as well as insulin-signaling related proteins.

No abstract

This study explored the effects of indole-3-carbinol on the proliferation of human nasopharyngeal carcinoma, both in vitro and in vivo, and the underlying mechanisms in inducing apoptosis of CNE1 cells. Proliferation, apoptosis, malondialdehyde, superoxide dismutase, glutathione peroxidase, expressions of caspase-9, and caspase-3 in human nasopharyngeal carcinoma cells CNE1 were examined. Indole-3-carbinol suppressed proliferation, induced apoptosis, decreased malondialdehyde level, increased the activity of superoxide dismutase and glutathione peroxidase, and up-regulated the expression of active fragments of caspase-9 and caspase-3 both in vitro and in vivo. It was concluded that indole-3-carbinol could inhibit proliferation and induce apoptosis of CNE1 cells and inhibit tumor growth in mice. Increased activity of superoxide dismutase and glutathione peroxidase and activated expression of caspase-9 and caspase-3 were also observed in indole-3-carbinol-treated tumors or tumor cells, suggesting that stress- and apoptosis-related molecules are involved in the indole-3-carbinol-induced apoptosis and inhibition of tumor growth.

Abstract:To evaluate scallop safety in the Guangzhou seafood market, contents of shellfish toxins in adductor muscle, mantle skirts, gills and visceral mass of scallops were examined using enzyme-linked immunosorbent assay (ELISA) and mouse unit assay. The results showed that: paralytic shellfish poisoning contents were up to 37.44 mg/100 g by ELISA and 319.99 MU/100 g by mouse unit assay, which did not exceed the limits of national standards (80 mg/100g and 400 MU/100 g); the contents of diarrhetic shellfish poisoning were 142.04 mg/100g and 0.2 MU/100 g, which exceeded the national standard limits (60 mg/100g); neurotoxic shellfish poisoning was undetectable; the contents of amnesic shellfish poisoning reached 220.12 mg/100g (no limit value could be referred to) . In addition, these poisons were present mainly in visceral mass and gills rather than adductor muscle and mantle skirts, suggesting that these toxins accumulate in a tissue-specific manner.