Preparation and bioactivity of the rare ginsenosides Rg3 and Rh2: An updated review.

Ginseng, an ancient medicinal herb, is used in oriental medicine for the treatment of various diseases. Saponins are the main bioactive components of ginseng, but the multiple glucosyl side chains on its molecules prevent ginsenosides from entering the blood through the intestinal membrane, thus reducing the efficacy. The preparation of rare ginsenosides, which are easy to be absorbed by human body and have higher drug activity, has been widely practiced by removing the sugar group of natural ginsenosides in vitro. Rare ginsenosides Rg3 and Rh2 have been approved as drugs or health supplements to improve immune function. This review summarizes the preparation methods of ginsenoside Rg3 and Rh2 in recent years. Ginsenoside Rg3 and Rh2 were prepared by biotransformation of protopanaxadiol type ginsenoside, with the highest conversion rate of 98.19% and 95.89% in the laboratory, respectively. At present, improving the conversion rate and reducing the production cost are still the bottleneck of industrial scale production of Rg3 and Rh2 through the deglycosylation directly from Rb1, Rb2, Rb3, Rc and Rd in the crude extract of ginseng. In addition, ginsenosides Rg3 and Rh2 play anti-inflammatory, anticancer, cardiovascular protective, immunomodulatory, neuroprotective, anti-diabetic, anti-fatigue, anti-allergic, anti-aging, antioxidant and other pharmacological effects by activating AMPK, JNK, NF-κB, MAPKs, P13K/AKT/mTOR and other signaling pathways. As potential drugs for prevention and treatment of various diseases, ginsenoside Rg3 and Rh2 need to further clarify other underlying mechanisms of action through in vitro and in vivo experiments.

Aqueous Extracts of Se-Enriched Auricularia auricular Exhibits Antioxidant Capacity and Attenuate Liver Damage in High-Fat Diet/Streptozotocin-Induced Diabetic Mice.

Oxidative stress triggered by hyperglycemia is thought to be a major factor in the development of liver disease during diabetes mellitus (DM). The aim of this study was to determine the antioxidant capacity of aqueous extracts of selenium-enriched Auricularia auricular (AESA) and further investigate the hepatic protection and potential mechanism of AESA in a mouse model of diabetes. An in vitro antioxidant assay confirmed that AESA exhibited better antioxidant capacity characterized by increased reducing power and scavenging capacity of free radicals, such as diphenyl picrylhydrazyl radical, hydroxyl radical, and superoxide radical. The diabetic model was induced by high-fat diet combined with a single injection of streptozotocin in C57BL/6 mice. Our results showed that AESA treatment improved diabetes-induced disorders of lipid metabolisms and alleviated liver damage in diabetic mice. Furthermore, the antioxidant enzyme activities of glutathione peroxidase and catalase in liver were increased and malondialdehyde level was decreased with AESA treatment compared with those in the DM group. In parallel, AESA significantly reduced the contents of tumor necrosis factor-alpha and interleukin-1beta in liver in comparison with the DM group. In addition, western blot results showed that the expression of receptor for advanced glycation end products (RAGE), phospho-c-Jun NH2-terminal kinase, phospho-extracellular signal-regulated kinase, and phospho-p38 kinase were remarkably decreased in AESA treatment group compared with DM group. Taken together, supplementation of AESA may effectively attenuate diabetic hepatopathology by exerting antioxidant function through the RAGE/mitogen-activated protein kinase pathway.

Reduction of Aflatoxin B1 Toxicity by Lactobacillus plantarum C88: A Potential Probiotic Strain Isolated from Chinese Traditional Fermented Food "Tofu".

In this study, we investigated the potential of Lactobacillus plantarum isolated from Chinese traditional fermented foods to reduce the toxicity of aflatoxin B1 (AFB1), and its subsequent detoxification mechanism. Among all the investigated L. plantarum strains, L. plantarum C88 showed the strongest AFB1 binding capacity in vitro, and was orally administered to mice with liver oxidative damage induced by AFB1. In the therapy groups, the mice that received L. plantarum C88, especially heat-killed L. plantarum C88, after a single dose of AFB1 exposure, showed an increase in unabsorbed AFB1 in the feces. Moreover, the effects of L. plantarum C88 on the enzymes and non-enzymes antioxidant abilities in serum and liver, histological alterations of liver were assayed. The results indicated that compared to the control group, L. plantarum C88 alone administration induced significant increase of antioxidant capacity, but did not induce any significant changes in the histological picture. Compared to the mice that received AFB1 only, L. plantarum C88 treatment could weaken oxidative stress by enhancing the activity of antioxidant enzymes and elevating the expression of Glutathione S-transferase (GST) A3 through Nuclear factor erythroid (derived factor 2) related factor 2 (Nrf2) pathway. Furthermore, cytochrome P450 (CYP 450) 1A2 and CYP 3A4 expression was inhibited by L. plantarum C88, and urinary aflatoxin B1-N7-guanine (AFB-N7-guanine), a AFB1 metabolite formed by CYP 1A2 and CYP 3A4, was significantly reduced by the presence of viable L. plantarum C88. Meanwhile, the significant improvements were showed in histological pictures of the liver tissues in mice orally administered with viable L. plantarum C88. Collectively, L. plantarum C88 may alleviate AFB1 toxicity by increasing fecal AFB1 excretion, reversing deficits in antioxidant defense systems and regulating the metabolism of AFB1.