Effects of the inhalation of the m3 receptor antagonist bencycloquidium bromide in a mouse cigarette smoke-induced airway inflammation model.

Bencycloquidium bromide (BCQB), a novel M3 receptor antagonist, alleviates airway hyperresponsiveness, inflammation, and airway remodeling in a murine model of asthma. The aim of this study was to investigate the anti-inflammatory activity of inhaled BCQB in a cigarette smoke (CS)-induced model of acute lung inflammation. Mice exposed to CS developed chronic obstructive pulmonary disease (COPD). Inhalation of BCQB suppressed the accumulation of neutrophils and macrophages in airways and lung and also inhibited the CS-induced increases in mRNA levels of keratinocyte-derived chemokine, monocyte chemotactic protein-1, tumor necrosis factor-alpha, and interleukin-1ß in lung and protein expression levels in bronchoalveolar lavage fluid. Moreover, BCQB (300 µg/ml) inhibited the CS-induced changes in superoxide dismutase and myeloperoxidase activities in the lungs. Our study suggests that BCQB might be a potential therapy for inflammation in CS-induced pulmonary diseases, including COPD.

Anti-fatigue and vasoprotective effects of quercetin-3-O-gentiobiose on oxidative stress and vascular endothelial dysfunction induced by endurance swimming in rats.

Chronic fatigue accumulation increases the incidence of cardiovascular disease while the treatment of antioxidants could prevent this development. We have previously shown that quercetin-3-O-gentiobiose (QG), a flavonoid isolated from tonic herb Okra, possesses anti-oxidative properties. In the present study, the protective effects of QG were evaluated in a rat model of load-induced endurance swimming. Oral administration of QG at the doses of 25-75mg/kg could significantly improve the endurance capability of rats to fatigue along with decrease serum lactic acid and blood urea nitrogen levels were decreased. Moreover, QG could alleviate vascular impairments, enhance the activities of antioxidant enzymes and attenuate the levels of inflammatory cytokines (MCP-1, IL-6 and TNF-α). The results indicated that QG had anti-fatigue and vasoprotective effects and represented a potential agent for the treatment of aortic pathology involved with fatigue- and related syndrome.

Antitumor and immunomodulatory effects of a water-soluble polysaccharide from Lilii Bulbus in mice.

Lilii Bulbus is a popular folk medicine in the worldwide and has attracted great attention due to its bioactivity against respiratory system diseases (include lung cancers). This study was the first report providing in vivo evidences of antitumor potential of the bioactive polysaccharide from Lilii Bulbus. One major fraction (LBP-1) was obtained by purifying the crude polysaccharides extracted from Lilii Bulbus. Chemical characterization analysis indicated that LBP-1 was only a glucan, whose average molecular weight was 30.5 kDa. Intraperitoneal administration of LBP-1 at the doses of 50-200mg/kg significantly inhibited the growth of Lewis lung carcinoma. Moreover, it could also obviously increase macrophage phagocytosis, splenocytes proliferation and cytokine (TNF-α, IL-2, IL-6 and IL-12) production to participate in the antitumor effects. LBP-1 could act as antitumor agent with immunomodulatory activity.

Cytotoxicity of epigallocatechin-3-gallate to LNCaP cells in the presence of Cu2+.

Epigallocatechin-3-gallate (EGCG) has shown remarkably anti-cancer activity, with its bioactivity being related to reactive conditions, such as pH and metal ions. The present study investigated the degradation of EGCG and its effect on prostate cancer cell in the presence of Cu2+. EGCG was incubated with prostate cancer cells, LNCaP, pretreated with or without Cu2+. EGCG in F-12 medium was quantified using HPLC and the viability of cells was assessed by gel electrophoresis, flow cytometry, and electron microscope. The results of HPLC showed that EGCG degraded completely within 12 h in F-12 medium with or without Cu2+. Gel electrophoresis and flow cytometry did not detect apoptosis of LNCaP cells when they were incubated with EGCG. Electron microscopy examination revealed that EGCG-Cu2+ complex led to damage of cytoplasm membrane in LNCaP cells. It was speculated that not EGCG, but its oxide and complex with Cu2+, are the bioactive components responsible for its cytotoxicity to LNCaP prostate cancer cells.