Green tea extract ameliorates macrophage-driven emphysematous lesions in chronic obstructive pulmonary disease induced by cigarette smoke condensate.

Chronic obstructive pulmonary disease (COPD) is an important lung disease characterized by complicated symptoms including emphysema. We aimed to explore the mechanisms underlying the protective effect of green tea extract (GTE) on cigarette smoke condensate (CSC)-induced emphysema by demonstrating the reduction of macrophage-induced protease expression through GTE treatment in vivo and in vitro. Mice were intranasally administered 50 mg/kg CSC once a week for 4 weeks, and doses of 100 or 300 mg/kg GTE were administered orally once daily for 4 weeks. GTE significantly reduced macrophage counts in bronchoalveolar lavage fluid and emphysematous lesions in lung tissues in CSC-exposed mice. In addition, GTE suppressed CSC-induced extracellular signal-regulated kinase (ERK)/activator protein (AP)-1 phosphorylation followed by matrix metalloproteinases (MMP)-9 expression as revealed by western blotting, immunohistochemistry, and zymography in CSC-instilled mice. These underlying mechanisms related to reduced protease expression were confirmed in NCI-H292 cells stimulated by CSC. Taken together, GTE effectively inhibits macrophage-driven emphysematous lesions induced by CSC treatment, and these protective effects of GTE are closely related to the ERK/AP-1 signaling pathway, followed by a reduced protease/antiprotease imbalance. These results suggest that GTE can be used as a supplementary agent for the prevention of emphysema progression in COPD patients.

Inner Shell of the Chestnut (Castanea crenatta) Suppresses Inflammatory Responses in Ovalbumin-Induced Allergic Asthma Mouse Model.

The inner shell of the chestnut (Castanea crenata) contains various polyphenols, which exert beneficial biological effects. Hence, we assessed the anti-inflammatory efficacy of a chestnut inner shell extract (CIE) in ovalbumin (OVA)-induced allergic asthma. We intraperitoneally injected 20 µg of OVA with 2 mg of aluminum hydroxide on days 0 and 14. On test days 21, 22, and 23, the mice were treated with aerosolized 1% (w/v) OVA in saline. CIE was administered orally at 100 and 300 mg/kg on days 18-23. CIE significantly reduced inflammatory cytokines and cells and immunoglobulin-E increased by OVA. Anti-inflammatory efficacy was revealed by reduction of inflammatory cell migration and mucus secretion in lung tissue. Further, CIE suppressed the OVA-induced nuclear factor kappa B (NF-κB) phosphorylation. Accordingly, the expression of cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS), and matrix metalloproteinase-9 (MMP-9) were decreased sequentially in lung tissues. CIE alleviated OVA-induced airway inflammation by restraining phosphorylation of NF-κB and the sequentially reduced expression of iNOS, COX-2, leading to reduced MMP-9 expression. These results indicate that CIE has potential as a candidate for alleviating asthma.

Prophylactic Catechin-Rich Green Tea Extract Treatment Ameliorates Pathogenic Enterotoxic Escherichia coli-Induced Colitis.

In this study, we explored the potential beneficial effects of green tea extract (GTE) in a pathogenic Escherichia coli (F18:LT:STa:Stx2e)-induced colitis model. The GTE was standardized with catechin and epigallocatechin-3-gallate content using chromatography analysis. Ten consecutive days of GTE (500 and 1000 mg/kg) oral administration was followed by 3 days of a pathogenic E. coli challenge (1 × 109 CFU/mL). In vitro antibacterial analysis showed that GTE successfully inhibited the growth of pathogenic E. coli, demonstrating over a 3-fold reduction under time- and concentration-dependent conditions. The in vivo antibacterial effect of GTE was confirmed, with an inhibition rate of approximately 90% when compared to that of the E. coli alone group. GTE treatment improved pathogenic E. coli-induced intestinal injury with well-preserved epithelial linings and villi. In addition, the increased expression of annexin A1 in GTE-treated jejunum tissue was detected, which was accompanied by suppressed inflammation-related signal expression, including TNFA, COX-2, and iNOS. Moreover, proliferation-related signals such as PCNA, CD44, and Ki-67 were enhanced in the GTE group compared to those in the E. coli alone group. Taken together, these results indicate that GTE has an antibacterial activity against pathogenic E. coli and ameliorates pathogenic E. coli-induced intestinal damage by modulating inflammation and epithelial cell proliferation.