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Aim. The study was conducted to investigate the antibacterial and antiasthmatic effects of Nandina domestica leaf extract, to find out its active components, and to assess its safety issue. Methods. (1) Solid-phase agar dilution method was used for antibacterial activity test of nandina leaf extract and the change of bacterial morphology after treatment was observed under the transmission microscope; (2) guinea pig model of asthma was used to test the asthma prevention effect of nandina leaf extract; (3) alkaloids and flavones were separated from nandina leaf extract and were further analyzed with HPLC-MS; (4) mice model was used to assessment of the safety issue of nandina leaf extract. Results. (1) Nandina leaf extract inhibited the growth of bacteria and destroyed bacterial membrane; (2) nandina leaf extract alleviated animal allergy and asthma; (3) the components reextracted by ethyl acetate were active, in which alkaloids inhibited Gram-positive bacteria and prevented asthma and flavones inhibited Gram-negative bacteria; (4) nandina leaf extract had no toxic effect on mice. Conclusion. Nandina leaves inhibit bacterial growth and prevent asthma through alkaloids and flavones, which had integrated function against chronic bronchitis. This study provided theoretical basement for producing new Chinese medicine against chronic bronchitis. [ABSTRACT FROM AUTHOR]

A hepatitis B virus (HBV) transgenic mice model was used to establish the fatty liver superimposed model by feeding the methionine choline-deficient (MCD) diet for 8 weeks, with or without the gavage of 2 mg/kg zeaxanthin dipalmitate (ZD) three times per week. Both wild-type and HBV transgenic mice, with MCD diet, gained typical non-obese non-alcoholic steatohepatitis (NASH) and HBV symptoms. Coadministration with ZD exhibited evident therapeutic effects through alleviating those pathological events. Moreover, long-term vehicle-ZD treatment was found to be safe. Thus, ZD is a promising and safe hepato-protective agent against hepatic injury induced by superimposed HBV and NASH in non-obese mice. [ABSTRACT FROM AUTHOR]

Oxidative stress has been increasingly recognized as a major contributing factor in a variety of human diseases, from inflammation to cancer. Although certain parts of signaling pathways are still under investigation, detailed molecular mechanisms for the induction of diseases have been elucidated, especially the link between excessive oxygen reactive species (ROS) damage and tumorigenesis. Emerging evidence suggests anti-oxidant therapy can play a key role in treating those diseases. Among potential drug resources, plant polysaccharides are natural anti-oxidant constituents important for human health because of their long history in ethnopharmacology, wide availability and few side effects upon consumption. Plant polysaccharides have been shown to possess anti-oxidant, anti-inflammation, cell viability promotion, immune-regulation and antitumor functions in a number of disease models, both in laboratory studies and in the clinic. In this paper, we reviewed the research progress of signaling pathways involved in the initiation and progression of oxidative stress- and cancer-related diseases in humans. The natural sources, structural properties and biological actions of several common plant polysaccharides, including Lycium barbarum, Ginseng, Zizyphus Jujuba, Astragalus lentiginosus, and Ginkgo biloba are discussed in detail, with emphasis on their signaling pathways. All of the mentioned common plant polysaccharides have great potential to treat oxidative stress and cancinogenic disorders in cell models, animal disease models and clinical cases. ROS-centered pathways (e.g. mitochondrial autophagy, MAPK and JNK) and transcription factor-related pathways (e.g. NF-B and HIF) are frequently utilized by these polysaccharides with or without the further involvement of inflammatory and death receptor pathways. Some of the polysaccharides may also influence tumorigenic pathways, such as Wnt and p53 to play their anti-tumor roles. In addition, current problems and future directions for the application of those plant polysaccharides are also listed and discussed. [ABSTRACT FROM AUTHOR]

Carthamus tinctorius L. is a multifunctional cash crop. Its flowers and seeds are extensively used in traditional herbal medicine in China, Korea, Japan, and other Asian countries, for treating various ailments such as gynecological, cardiovascular, and cerebrovascular diseases as well as blood stasis and osteoporosis. More than 100 compounds have been isolated and identified from C. tinctorius. Flavonoids and alkaloids, especially the quinochalcone c-glycoside hydroxysafflor yellow A, N-( p-Coumaroyl)serotonin, and N-feruloylserotonin, are responsible for most of the pharmacological activities of C. tinctorius. In this paper, comprehensive and up-to-date information on the phytochemistry and pharmacology of C. tinctorius is presented. This information will be helpful for further explorations of the therapeutic potential of C. tinctorius and may provide future research opportunities. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Lycium barbarum has been used as a traditional Chinese medicine to nourish liver, kidneys and the eyes. Aim of the study: We investigated the protective mechanisms of Wolfberry, Lycium barbarum polysaccharides (LBP) in carbon tetrachloride (CCl4)-induced acute liver injury. Materials and methods: Mice were intraperitoneally injected with a 50μl/kg CCl4 to induce acute hepatotoxicity (8h) and were orally fed with LBP 2h before the CCl4 injection. There were six experimental groups of mice (n =7–8 per group), namely: control mice (vehicle only; 1mg/kg LBP or 10mg/kg LBP), CCl4-treated mice and CCl4 +LBP treated mice (1mg/kg LBP or 10mg/kg LBP). Results: Pre-treatment with LBP effectively reduced the hepatic necrosis and the serum ALT level induced by CCl4 intoxication. LBP remarkably inhibited cytochrome P450 2E1 expression and restored the expression levels of antioxidant enzymes. It also decreased the level of nitric oxide metabolism and lipid peroxidation induced by CCl4. LBP attenuated hepatic inflammation via down-regulation of proinflammatory mediators and chemokines. Furthermore, LBP promoted liver regeneration after CCl4 treatment. The protective effects of LBP against hepatotoxicity were partly through the down-regulation of nuclear factor kappa-B activity. Conclusion: LBP is effective in reducing necroinflammation and oxidative stress induced by a chemical toxin, thus it has a great potential use as a food supplement in the prevention of hepatic diseases. [Copyright &y& Elsevier]

The article offers information on the study conducted on the chemical composition and therapeutic significance of Edgeworthia chrysantha. It was found that the plant is a member of the Thymelaeaceae family in Eastern Asia. When researchers did a chemical analysis on the plant, it contains coumarins triterpenes and flavonoids. It has several uses which include making paper in Japan, flowers are used in the anti-bacterial crud drug known as Meng hua, and its barks and stems as folkloric medicine.

Gogi berry is a traditional food supplement and medical herbal which has been widely used in Eastern Asian countries. Lycium barbarum polysaccharides (LBP) are the major active components of Gogi berry and have been proved to possess a lot of biological activities. We aimed to delineate the protective effect and mechanism of LBP on hepatic encephalopathy (HE). We investigated the protective mechanism of LBP in a thioacetamide (TAA, intraperitoneally injected, 400 mg/kg) induced acute HE mice model. Key phenotypes of clinical HE were phenocopied in the mice model, including high mortality, severe hepatic histology injury, increased hepatic oxidative stress, apoptosis, enhanced circulating levels of pro-inflammatory cytokines and ammonia, suppressed tryptophan hydroxylase activity, and deficits in locomotor activity. The pathological alterations were effectively ameliorated by the oral administration with LBP (5 mg/kg, oral gavage, everyday), which were mediated by regulating MAPK pathways in both the liver and brain. Knockout of pro-inflammatory cytokines TNF-α or IL-6 effectively ameliorated impaired mice locomotor activity and MAPK activation in the brain. In an in vitro TNF-α-, IL-6-, or ammonia-induced microglia damaged cell model, cell injuries were evidently protected by the co-administration with LBP (50 μg/ml). LBP ameliorated the hepatic/brain injuries and impaired locomotor activities in a HE mice model. Pro-inflammatory cytokines may serve as communicating molecules linking the liver and brain for the HE pathogenesis, partly through MAPK regulation. Hepatic encephalopathy is a neuropsychiatric disease caused by severe liver damages or failure. In the present study, we found that LBP ameliorate HE symptoms by attenuating the pro-inflammatory cytokine production and disturbed MAPK pathway in the liver and brain. TNF-α and IL-6 may serve as communicating molecules linking the liver and brain for the HE pathogenesis, partly through MAPK regulation. Image 1 [ABSTRACT FROM AUTHOR]