Puerarin is the major bioactive ingredient isolated from the root of the Pueraria lobata (Willd.) Ohwi, which is well known as Gegen (Chinese name) in traditional Chinese medicine. As the most abundant secondary metabolite, puerarin was isolated from Gegen in the late 1950s. Since then, its pharmacological properties have been extensively investigated. It is available in common foods and is used in alternative medicine. It has been widely used in the treatment of cardiovascular and cerebrovascular diseases, diabetes and diabetic complications, osteonecrosis, Parkinson's disease, Alzheimer's disease, endometriosis, and cancer. The beneficial effects of puerarin on the various medicinal purposes may be due to its wide spectrum of pharmacological properties such as vasodilation, cardioprotection, neuroprotection, antioxidant, anticancer, antiinflammation, alleviating pain, promoting bone formation, inhibiting alcohol intake, and attenuating insulin resistance. However, the direct molecular mechanisms and targets remain unclear. This review provides a comprehensive summary of the pharmacological effects of puerarin.

Portulaca oleracea L., belonging to the Portulacaceae family, is commonly known as purslane in English and Ma-Chi-Xian in Chinese. It is a warm-climate, herbaceous succulent annual plant with a cosmopolitan distribution. It is eaten extensively as a potherb and added in soups and salads around the Mediterranean and tropical Asian countries and has been used as a folk medicine in many countries. Diverse compounds have been isolated from Portulaca oleracea, such as flavonoids, alkaloids, polysaccharides, fatty acids, terpenoids, sterols, proteins vitamins and minerals. Portulaca oleracea possesses a wide spectrum of pharmacological properties such as neuroprotective, antimicrobial, antidiabetic, antioxidant, anti-inflammatory, antiulcerogenic, and anticancer activities. However, few molecular mechanisms of action are known. This review provides a summary of phytochemistry and pharmacological effects of this plant.

As an important source for traditional medical systems such as Ayurvedic medicine and traditional Chinese medicine, herbal medicines have received widespread attentions from all over the world, especially in developing countries. Over the past decade, studies on gut microbiota have generated rich information for understanding how gut microbiota shape the functioning of our body system. In view of the importance of gut microbiota, the researchers engaged in studying herbal medicines have paid more and more attention to gut microbiota and gut microbiota metabolites. Among a variety of gut microbiota metabolites, short-chain fatty acids (SCFAs) have received most attention because of their important role in maintaining the hemostasis of hosts and recovery of diseases. Herbal medicines, as an important resource provider for production of SCFAs, have been demonstrated to be able to modulate gut microbiota composition and regulate SCFAs production. In this mini-review, we summarize current knowledge about SCFAs origination, the role of SCFAs in health and disease, the influence of herbal medicine on SCFAs production and the corresponding mechanisms. At the end of this review, the strategies and suggestions for further research of SCFAs and herbal medicines are also discussed.

No abstract

Context: Polydatin, also named piceid (3,4 0 ,5-trihydroxystilbene-3-b-D-glucoside, PD), is a monocrystalline compound isolated from Polygonum cuspidatum Sieb. et Zucc. (Polygonaceae), but is also detected in grape, peanut, hop cones, red wines, hop pellets, cocoa-containing products, chocolate products and many daily diets. There are numerous investigations reported of PD in the past 22 years, but they are usually scattered across various publications, which may block further research and clinical use of PD. Objective: The article summarizes and evaluates the published scientific information of PD pharmacological effects and pharmacokinetics since 1990. Materials and methods: The information from 98 cases included in this review was compiled using major databases such as MEDLINE, Elsevier, Springer, PubMed, Scholar and CNKI. Results: Numerous pharmacological investigations of PD mainly focus on cardiovascular effects, neuroprotection, anti-inflammatory and immunoregulatory effects, anti-oxidation, anti-tumor, liver and lung protection, etc. Conclusion: A great number of pharmacological and pharmacokinetic investigations in the past 22 years have demonstrated that PD has favorable therapeutic properties, indicating its potential as an effective material. However, further research is needed to explore its molecular mechanisms of action and definitive target proteins.

No abstract

The Western meat-rich diet is both high in protein and fat. Although the hazardous effect of a high fat diet (HFD) upon liver structure and function is well recognized, whether the co-presence of high protein intake contributes to, or protects against, HF-induced hepatic injury remains unclear. Increased intake of branched chain amino acids (BCAA, essential amino acids compromising 20% of total protein intake) reduces body weight. However, elevated circulating BCAA is associated with non-alcoholic fatty liver disease and injury. The mechanisms responsible for this quandary remain unknown; the role of BCAA in HF-induced liver injury is unclear. Utilizing HFD or HFD + BCAA models, we demonstrated BCAA supplementation attenuated HFD-induced weight gain, decreased fat mass, activated mammalian target of rapamycin (mTOR), inhibited hepatic lipogenic enzymes, and reduced hepatic triglyceride content. However, BCAA caused significant hepatic damage in HFD mice, evidenced by exacerbated hepatic oxidative stress, increased hepatic apoptosis, and elevated circulation hepatic enzymes. Compared to solely HFD-fed animals, plasma levels of free fatty acids (FFA) in the HFD + BCAA group are significantly further increased, due largely to AMPKα2-mediated adipocyte lipolysis. Lipolysis inhibition normalized plasma FFA levels, and improved insulin sensitivity. Surprisingly, blocking lipolysis failed to abolish BCAA-induced liver injury. Mechanistically, hepatic mTOR activation by BCAA inhibited lipid-induced hepatic autophagy, increased hepatic apoptosis, blocked hepatic FFA/triglyceride conversion, and increased hepatocyte susceptibility to FFA-mediated lipotoxicity. These data demonstrated that BCAA reduces HFD-induced body weight, at the expense of abnormal lipolysis and hyperlipidemia, causing hepatic lipotoxicity. Furthermore, BCAA directly exacerbate hepatic lipotoxicity by reducing lipogenesis and inhibiting autophagy in the hepatocyte.

No abstract