Xinwei Jiang

Cytoprotective effects of dietary flavonoids against cadmium‐induced toxicity

Cadmium (Cd) damages the liver, kidney, bones, reproductive system, and other organs. Flavonoids, such as anthocyanins and flavonols, which are commonly found in plant foods, have shown protective effects against Cd‐induced damage. The cytoprotective effects of flavonoids against Cd‐induced diseases are mainly attributable to three mechanisms. First, flavonoids clear reactive oxygen species, thereby reducing lipid peroxide production and improving the activity of antioxidation enzymes. Second, flavonoids chelate Cd, thus reducing the accumulation of Cd and altering the levels of other essential metal ions in vivo. Third, flavonoids reduce DNA damage and inhibit apoptosis. In addition, flavonoids were found to inhibit inflammation and fibrosis and improve glycometabolism and the secretion of reproductive hormones. We introduce the daily dosage and absorption rate of flavonoids and then focus on their bioactive effects against Cd‐induced toxicity and reveal the underlying metabolic pathway, which provides a basis for further study of the nutritional prevention of Cd‐induced injury. In particular, a better understanding is needed of the structure–activity relationship of flavonoids against Cd toxicity, which has not yet been reported.

Protective Effect of Cyanidin-3-O-Glucoside against Ultraviolet B Radiation-Induced Cell Damage in Human HaCaT Keratinocytes.

Ultraviolet radiation is the major environmental harmful factor that has emotional impact on human skin. The aim of the present study was to determine the mechanism of protection of cyanidin-3-O-glucoside against ultraviolet B (UVB)-induced damage to human HaCaT keratinocytes. Our results show that cyanidin-3-O-glucoside decreased the levels of intracellular reactive oxygen species generated by UVB treatment. Cyanidin-3-O-glucoside also decreased the UVB-augmented levels of the DNA damage indicators phospho-p53 and phospho-ATM/ATR. In addition, cyanidin-3-O-glucoside protected keratinocytes from UVB-induced injury by overturning the disruption of mitochondrial membrane potential and reversing apoptosis. The expression of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) was attenuated in UVB-exposed cells but restored in UVB/cyanidin-3-O-glucoside-treated cells. Furthermore, expression of the proapoptotic proteins Bcl-2-associated X (Bax) and the key apoptosis executer cleaved caspase-3 were increased in UVB-irradiated cells and decreased in UVB/cyanidin-3-O-glucoside-treated cells. For these reasons, the results demonstrate that cyanidin-3-O-glucoside protects human keratinocytes against UVB-induced oxidative stress and apoptosis. Our study provides a theoretical basis for the use of cyanidin-3-O-glucoside in the fight against light damage.

Cyanidin-3-O-Glucoside Protects against 1,3-Dichloro-2-Propanol-Induced Reduction of Progesterone by Up-regulation of Steroidogenic Enzymes and cAMP Level in Leydig Cells

1,3-Dichloro-2-propanol (1,3-DCP) is a food processing contaminant and has been shown to perturb male reproductive function. Cyanidin-3-O-glucoside (C3G), an anthocyanin antioxidant, is reported to have protective effects on many organs. However, it remains unclear whether C3G protects against chemical-induced reproductive toxicity. The present study was therefore to investigate the intervention of C3G on 1,3-DCP-induced reproductive toxicity in R2C Leydig cells. Results demonstrated that C3G inhibited the 1,3-DCP-induced cytotoxicity and cell shape damage with the effective doses being ranging from 10 to 40 μmol/L. In addition, 1,3-DCP (2 mmol/L) exposure significantly increased the ROS level and mitochondrial membrane potential damage ratio, leading to a decrease in progesterone production, while C3G intervention reduced the ROS level, and increased the progesterone production after 24 h treatment. Most importantly, C3G intervention could up-regulate the cyclic adenosine monophosphate (cAMP) level and protein expression of steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase. It was concluded that C3G is effective in reducing 1,3-DCP-induced reproductive toxicity via activating steroidogenic enzymes and cAMP level.

Cyanidin-3-O-glucoside inhibits the UVB-induced ROS/COX-2 pathway in HaCaT cells

Ultraviolet (UV) radiation from sunlight, especially UVB (290-320nm), is one of the most important environmental factors that destroys the integrity of the skin and causes epidermal cell apoptosis, potentially even leading to skin cancer. UVB irradiation can cause skin damage by stimulating inflammatory and apoptotic pathways. Anthocyanins are flavonoids that are common in many vegetable foods, and have also demonstrated chemopreventive effects. Cyanidin-3-O-glucoside, as a typical anthocyanin, exhibits anti-inflammatory and anti-oxidant effects. This study aimed to investigate the effects, as well as the underlying mechanisms, of treating UVB-exposed HaCaT cells with Cyanidin-3-O-glucoside. We demonstrated that Cyanidin-3-O-glucoside could effectively prevent the UVB-induced apoptosis of HaCaT cells. This protective effect can be explained by the scavenging of ROS and the suppression of COX-2 expression by interaction with the MAPK and Akt signaling pathways. Furthermore, we used Celecoxib as a positive control, and results showed that Cyanidin-3-O-glucoside was more effective at decreasing EGFR phosphorylation than Celecoxib, which translated into a stronger inhibitory effect against the downstream elements p38, ERK, and JNK. Taken together, these results indicate that Cyanidin-3-O-glucoside can protect HaCaT cells against UVB radiation, which could provide a basis for the development of a potent nutritional therapy for UVB-induced skin disorders.

Protection of cyanidin-3-O-glucoside against acrylamide- and glycidamide-induced reproductive toxicity in leydig cells

Acrylamide (AA) occurs in many cooked carbohydrate-rich foods and has caused widespread concern as a possible carcinogen. Glycidamide (GA) is the ultimate genotoxic metabolite of AA. The present study was to investigate the protective effect of Cyanidin-3-O-glucoside (C3G) against AA- and GA-induced reproductive toxicity in R2C Leydig cells. The results demonstrated that C3G inhibited AA- and GA-induced cytotoxicity and mitochondria-mediated cell apoptosis, the effective doses of C3G were ranging from 10 to 50 μM. Besides, AA (1.925 mM) and GA (0.872 mM) exposure increased ROS level and decreased mitochondrial membrane potential, which led to a decrease in progesterone production, while C3G ranging from 10 to 50 μM reduced ROS immediately, and increased progesterone production after 24 h treatment. Furthermore, C3G up-regulated expression of Bcl-2 protein and down-regulated pro-apoptotic protein Bax and cleaved Caspase-3 after 24 h treatment in 1.925 mM AA- and 0.872 mM GA-treated R2C cells. Moreover, C3G intervention increased the protein expression of steroidogenic acute regulatory (StAR). It was concluded that C3G is effective in reducing AA- and GA-induced reproductive toxicity via inhibition of ROS generation, mitochondrial membrane depolarization and apoptosis, as well as activating steroidogenic enzymes.

6-Gingerol Regulates Hepatic Cholesterol Metabolism by Up-regulation of LDLR and Cholesterol Efflux-Related Genes in HepG2 Cells

Gingerols, the pungent ingredients in ginger, are reported to possess a cholesterol-lowering activity. However, the underlying mechanism remains unclear. The present study was to investigate how 6-gingerol (6-GN), the most abundant gingerol in fresh ginger, regulates hepatic cholesterol metabolism. HepG2 cells were incubated with various concentrations of 6-GN ranging from 50 to 200 μM for 24 h. Results showed that both cellular total cholesterol and free cholesterol decreased in a dose-dependent manner. Besides, 6-GN ranging from 100 to 200 μM increased the LDLR protein and uptake of fluorescent-labeled LDL. Moreover, the mRNA and protein expressions of cholesterol metabolism-related genes were also examined. It was found that 6-GN regulated cholesterol metabolism via up-regulation of LDLR through activation of SREBP2 as well as up-regulation of cholesterol efflux-related genes LXRα and ABCA1.

Toxic effects of zearalenone on gametogenesis and embryonic development: A molecular point of review

Zearalenone is commonly generated from moldy cereal grain, which is toxic to the development of gametogenesis and embryo in human and animals. The zearalenone-induced reproductive damage is mainly attributed to four mechanisms. Firstly, zearalenone as an oestrogen-like compound binds to estrogen receptor and causes damage to germ cells and testicular structure. Secondly, zearalenone disrupts the blood-testis barrier, and causes the damage to germ cells. Thirdly, zearalenone elevates oxidative stress, which increases the production of lipid peroxides, and results in the damage to the antioxidant defense system. Fourth, zearalenone increases DNA damage and promotes cells apoptosis. In addition, Zearalenone induces inflammatory reactions and leads to the disorders of reproductive hormones. In this study, we systematically introduced the toxic effects of zearalenone on gametogenesis and embryonic development in animals, and focused on the molecular pathways, which providing a basis for further prevention of zearalenone-induced injury.

Recent advances of medical foods in China: The opportunities and challenges under standardization

Malnutrition with high incidence in hospitalized patients in China has brought a significant burden of disease. Although many clinical studies have demonstrated the importance of nutritional for patients with malnutrition, the application of medical foods in China is still restricted. For the classification, limits, production and registration of medical foods, the Chinese government newly enacted a series of regulations. In this review, comparing the policy, researches, and product variety of medical foods in China with other countries, although the current status of the development of medical foods in China is still far behind that of developed countries, some of regulations are stricter than those of many other countries or organizations. The medical foods in China are divided into four categories, the nutrients and environmental contaminants are limited to ensure the safety. As a prospect, the development of medical foods in China is expected to get out of the predicament of lack of emphasis, shortage of supply, backward of local processing technology and the imperfect management system. After all, in view of the huge population and the increasing demand of nutrition in China, there must be a very good prospect for the future development of the medical foods industry in China.

The target cells of anthocyanins in metabolic syndrome

Abstract Metabolic syndrome develops to several related chronic diseases, such as obesity, cardiovascular disease, hypertension, diabetes, and fatty liver disease. Diseases are outcomes of various cells dysfunction, which are especially acting with a network in metabolic syndrome. Anthocyanins are natural edible pigments widely existed in dark-colored fruits, vegetables, and grains. Epidemiological investigation and nutritional intervention of anthocyanins have exhibited broad-spectrum biological effects that they can benefit patients with metabolic syndrome related chronic diseases. Whereas the underlying mechanisms and the effects of anthocyanins on critical cells in chronic metabolic diseases are complex and elusive. Therefore, this review summarizes the studies about the effects of anthocyanins on various metabolism related chronic diseases, and mainly focuses on the effects and underlying molecular mechanisms on critical cells. We confirmed that anthocyanins are efficient on adipocytes, endothelial cells, inflammatory cells, hepatocytes, intestinal cells and gut microbiota, but lack of evidence on platelets, skeletal muscle cells, hepatic stellate cells and pancreatic beta cells. Additionally, we discussed the structure-function relationship of anthocyanins and the metabolites. This review summarizes the development of studies on anthocyanins with its target cells in metabolic syndrome, and discusses the unclear aspects of the anthocyanins research work, which is necessary for the future clinical application.