Preventive effects of tea and tea catechins against influenza and acute upper respiratory tract infections: a systematic review and meta-analysis.

PURPOSE: Gargling with tea has protective effects against influenza infection and upper respiratory tract infection (URTI). To evaluate if tea and tea catechin consumption has the same protective effects as gargling with tea, we performed a systematic review and meta-analysis. METHODS: We performed a comprehensive literature search using the PubMed, Cochrane Library, Web of Science, and Ichu-shi Web databases. The search provided six randomized controlled trials (RCTs) and four prospective cohort studies (n = 3748). The quality of each trial or study was evaluated according to the Cochrane risk-of-bias tool or Newcastle-Ottawa Scale. We collected data from publications meeting the search criteria and conducted a meta-analysis of the effect of tea gargling and tea catechin consumption for preventing URTI using a random effects model. RESULTS: Tea gargling and tea catechin consumption had significant preventive effects against URTI (risk ratio [RR] = 0.74, 95% confidence interval [CI] 0.64-0.87). In sub-analyses, a significant preventive effect was observed by study type (prospective cohort study: RR = 0.67, 95% CI 0.50-0.91; RCT: RR = 0.79, 95% CI 0.66-0.94) and disease type (influenza: RR = 0.69, 95% CI 0.58-0.84; acute URTI: RR = 0.78, 95% CI 0.62-0.98). Both gargling with tea and consuming tea catechins effectively protected against URTI (tea and tea catechins consumption: RR = 0.68, 95% CI 0.52-0.87; tea gargling: RR = 0.83, 95% CI 0.72-0.96). CONCLUSION: Our findings suggest that tea gargling and tea catechin consumption may have preventive effects against influenza infection and URTI. The potential effectiveness of these actions as non-pharmaceutical interventions, however, requires further investigation.

Rhododendrol, a depigmentation-inducing phenolic compound, exerts melanocyte cytotoxicity via a tyrosinase-dependent mechanism.

Rhododendrol, an inhibitor of melanin synthesis developed for lightening/whitening cosmetics, was recently reported to induce a depigmentary disorder principally at the sites of repeated chemical contact. Rhododendrol competitively inhibited mushroom tyrosinase and served as a good substrate, while it also showed cytotoxicity against cultured human melanocytes at high concentrations sufficient for inhibiting tyrosinase. The cytotoxicity was abolished by phenylthiourea, a chelator of the copper ions at the active site, and by specific knockdown of tyrosinase with siRNA. Hence, the cytotoxicity appeared to be triggered by the enzymatic conversion of rhododendrol to active product(s). No reactive oxygen species were detected in the treated melanocytes, but up-regulation of the CCAAT-enhancer-binding protein homologous protein gene responsible for apoptosis and/or autophagy and caspase-3 activation were found to be tyrosinase dependent. These results suggest that a tyrosinase-dependent accumulation of ER stress and/or activation of the apoptotic pathway may contribute to the melanocyte cytotoxicity.