Aug 2026· Frontiers in Nutrition· Vol 13· 0 citations· 67 references
Medicine
TL;DR
It is demonstrated that tea leaves infected with tea blister blight disease, rather than being discarded or managed solely through fungicide application, can be valorized as a bioactive-enriched resource for applications in functional nutrition and health-promoting products.
Abstract
Background Oxidative stress and inflammation play key pathological mechanisms involved in the development of chronic diseases. Although tea blister blight reduces commercial tea quality, pathogen-induced stress may enhance the accumulation of bioactive phenolics and flavonoids, making infected leaves a potential resource for the food-medicine homology framework. This study aimed to evaluate the protective effects of a tea blister blight aqueous extract (TBB) against copper sulfate (CuSO4)-induced oxidative and inflammatory stress in zebrafish (Danio rerio) embryos. Methods Zebrafish embryos were exposed to 3 μM CuSO4 and co-treated with TBB at concentrations of 0.3–0.9 mg/mL. Developmental toxicity was evaluated based on survival, hatching, and morphological outcomes. Oxidative stress was assessed by measuring malondialdehyde (MDA) levels and antioxidant enzyme activities, including superoxide dismutase (SOD) and catalase (CAT). The expression of genes related to antioxidant defense, inflammation, and apoptosis was also analyzed. Results TBB treatment significantly increased embryo survival by 12.74–15.81% and the hatching rate by 46.12–51.38% than the CuSO4-exposed group. TBB also reduced CuSO4-induced developmental toxicity by increasing body length by 15.38–16.35% and improving the sinus venosus–bulbus arteriosus distance by 10.40–14.80%. In addition, TBB significantly mitigated oxidative stress by reducing MDA levels by 16.74–25.61% and enhancing SOD and CAT activities by 31.29–72.35% and 69.66–92.37%, respectively. Gene expression analysis showed that TBB upregulated antioxidant-related genes (Mn-sod, CAT, and Gpx1a), suppressed proinflammatory genes (TNF-α, NF–κB, NLRP3, and IL-1β), and downregulated the pro-apoptotic gene bax, while enhancing anti-inflammatory (IL-10) and anti-apoptotic (Bcl-2) expression. Conclusion These findings demonstrate that TBB provides multilevel biological protection through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. Importantly, this study provides a new perspective by demonstrating that tea leaves infected with tea blister blight disease, rather than being discarded or managed solely through fungicide application, can be valorized as a bioactive-enriched resource for applications in functional nutrition and health-promoting products.
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