[Comprehensive Review on Environmental Biogeochemistry of Nonylphenol and Suggestions for the Management of Emerging Contaminants].

In recent years, China's air environment, water environment, and soil environmental quality have been improved, and a "clear water blue sky" has become a normal state. However, as persistent organic pollutants, endocrine-disrupting chemicals, antibiotics, microplastics, and other emerging contaminants are continuously detected in the environment, these emerging contaminants have gradually been attracting wide attention. Nonylphenol, as a typical endocrine disrupting chemical, has also attracted the attention of researchers. The environmental behaviors and exposure levels of nonylphenol in Chinese water bodies were summarized systematically, and the ecological risks caused by nonylphenol were evaluated based on the risk quotient method and joint probability curve method. The results showed that the toxic effects of nonylphenol on aquatic organisms mainly included acute toxicity, growth and development toxicity, and estrogenic effect and reproductive toxicity. Nonylphenol was commonly found in the water bodies of major drainage areas in China, and the average concentration of nonylphenol ranged from 60 to 1000 ng·L-1, with the highest concentration being as high as 4628 ng·L-1. The results of risk assessment based on the risk quotient method and joint probability curve method showed that nonylphenol had certain risks to aquatic life in the major basins of China. Finally, the commonly used nonylphenol treatment, disposal, and risk management and control technologies were summarized, and the international supervision methods of endocrine-disrupting chemicals were compared. Aiming at addressing the problems existing in China's environmental management, targeted policy suggestions were put forward. The research results can provide reference for the management and control of emerging contaminants in China.

6-Shogaol Protects against Oxidized LDL-Induced Endothelial Injruries by Inhibiting Oxidized LDL-Evoked LOX-1 Signaling.

Endothelial dysfunction and oxLDL are believed to be early and critical events in atherogenesis. 6-Shogaol is the major bioactive compound present in Zingiber officinale and possesses the anti-atherosclerotic effect. However, the mechanisms remain poorly understood. The goal of this study was to investigate the effects of 6-shogaol on oxLDL-induced Human umbilical vein endothelial cells (HUVECs) injuries and its possible molecular mechanisms. Hence, we studied the effects of 6-shogaol on cell apoptosis, cellular reactive oxygen species (ROS), NF- κ B activation, Bcl-2 expression, and caspase -3, -8, -9 activities. In addition, E-selectin, MCP-1, and ICAM-1 were determined by ELISA. Our study show that oxLDL increased LOX-1 expression, ROS levels, NF- κ B, caspases-9 and -3 activation and decreased Bcl-2 expression in HUVECs. These alterations were attenuated by 6-shogaol. Cotreatment with 6-shogaol and siRNA of LOX-1 synergistically reduced oxLDL-induced caspases -9, -3 activities and cell apoptosis. Overexpression of LOX-1 attenuated the protection by 6-shogaol and suppressed the effects of 6-shogaol on oxLDL-induced oxidative stress. In addition, oxLDL enhanced the activation of NF- κ B and expression of adhesion molecules. Pretreatment with 6-shogaol, however, exerted significant cytoprotective effects in all events. Our data indicate that 6-shogaol might be a potential natural antiapoptotic agent for the treatment of atherosclerosis.

Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2.

AIM OF THE STUDY: Vessel endothelium injury caused by reactive oxygen species (ROS) including H(2)O(2) plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, agents or antioxidants that can inhibit production of ROS has highly clinical values in cardiovascular therapy. Curculigoside is the major bioactive compounds present in Curculigo orchioides, and possess potent antioxidant properties against oxidative stress insults through undefined mechanism(s). The present study was designed to test the hypothesis that curculigoside can inhibit H(2)O(2)-induced injury in human umbilical vein endothelial cells. MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with curculigoside in the presence/absence of hydrogen peroxide (H(2)O(2)). The protective effects of curculigoside OP-D against H(2)O(2) were evaluated. RESULTS: HUVECs incubated with 400 µM H(2)O(2) had significantly decreased the viability of endothelial cells, which was accompanied with apparent cells apoptosis, the activation of caspase-3 and the upregulation of p53 mRNA expression. In addition, H(2)O(2) treatment induced a marked increase of MDA, LDH content and in intracellular ROS, decreased the content of nitric oxide (NO) and GSH-Px activities in endothelial cells. However, pretreatment with 0.5.5,10 µM curculigoside resulted in a significant recovery from H(2)O(2)-induced cell apoptosis. Also, it decreased other H(2)O(2)-induced damages in a concentration-dependent manner. Furthermore, pretreatment with curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H(2)O(2)-induced cell apoptosis. CONCLUSION: The present study shows that curculigoside can protect endothelial cells against oxidative injury induced by H(2)O(2), suggesting that this compound may constitute a promising intervention against cardiovascular disorders.

Protective effects of silybin on human umbilical vein endothelial cell injury induced by H2O2 in vitro.

Oxidative injury induces cellular and nuclear damages that lead to cell injury. Agents or antioxidants that can inhibit production of reactive oxygen species can prevent injury. We tested the hypothesis that silybin can inhibit H2O2-induced injury in human umbilical vein endothelial cells. Eighteen hours of treatment with 750 micromol l(-1) H2O2 significantly stimulated expression of caspase-3 and cell apoptosis. In addition, it is observed that H2O2 increased the amounts of malondialdenhyde (MDA), the dehydrogenase (LDH) leakage, and decreased the activity of GSH-Px and NO contents in ECV-304 cells. In the H2O2 apoptosis model, the addition of 6.25-25 mg/L of silybin, which has in vitro radical scavenging activity, partially restored cell viability with a reduction in H2O2-induced apoptotic DNA damage, and decreased the expression of caspase-3. Moreover, it decreased other H2O2-induced damage in a concentration-dependent manner. The endothelial cell apoptosis was detected by AO/EB dual staining as well as flow cytometry, and the activity of pro-apoptotic factor caspase-3 was detected by immunocytochemical method. Our results suggest that the antioxidant, silybin, protects ECV-304 cells against H2O2-induced injury probably through its antioxidant activity, increasing the NO content, the activity GSH-Px and inhibiting signaling pathways mediated by caspase-3.