Camellia sinensis polysaccharide attenuates inflammatory responses via the ROS-mediated pathway by endocytosis.

Polysaccharide CSTPs extracted from Camellia sinensis tea-leaves possessed unique against oxidative damage by scavenging ROS. Herein, acid tea polysaccharide CSTPs-2 with tightly packed molecular structure was isolated, purified and characterized in this research. Furthermore, the effects of CSTPs-2 on ROS-involved inflammatory responses and its underlying mechanisms were investigated. The results suggest that CSTPs-2 dramatically reduced the inflammatory cytokines overexpression and LPS-stimulated cell damage. CSTPs-2 could trigger the dephosphorylation of downstream AKT/MAPK/NF-κB signaling proteins and inhibit nuclear transfer of p-NF-κB to regulate the synthesis and release of inflammatory mediators in LPS-stimulated cells by ROS scavenging. Importantly, the impact of CSTPs-2 in downregulating pro-inflammatory cytokines and mitigating ROS overproduction is associated with clathrin- or caveolae-mediated endocytosis uptake mechanisms, rather than TLR-4 receptor-mediated endocytosis. This study presents a novel perspective for investigating the cellular uptake mechanism of polysaccharides in the context of anti-inflammatory mechanisms.

A Temperature-Dependent Model for Tritrophic Interactions Involving Tea Plants, Tea Green Leafhoppers and Natural Enemies.

The tea green leaf hopper, Empoasca onukii Matsuda, is a severe pest of tea plants. Volatile emissions from tea shoots infested by the tea green leafhopper may directly repel insect feeding or attract natural enemies. Many studies have been conducted on various aspects of the tritrophic relationship involving tea plants, tea green leafhoppers and natural enemies. However, mathematic models which could explain the dynamic mechanisms of this tritrophic interaction are still lacking. In the current work, we constructed a realistic and stochastic model with temperature-dependent features to characterize the tritrophic interactions in the tea agroecosystem. Model outputs showed that two leafhopper outbreaks occur in a year, with their features being consistent with field observations. Simulations showed that daily average effective accumulated temperature (EAT) might be an important metric for outbreak prediction. We also showed that application of slow-releasing semiochemicals, as either repellents or attractants, may be highly efficacious for pest biocontrol and can significantly increase tea yields. Furthermore, the start date of applying semiochemicals can be optimized to effectively increase tea yields. The current model qualitatively characterizes key features of the tritrophic interactions and provides critical insight into pest control in tea ecosystems.

Modeling the neuro-protection of theaflavic acid from black tea and its synergy with nimodipine via mitochondria apoptotic pathway.

Ischemic stroke presents a leading cause of mortality and morbidity worldwide. Theaflavic acid (TFA) is a theaflavin isolated from black tea that exerts a potentially neuro-protective effect. However, the dynamic properties of TFA-mediated protection remain largely unknown. In the current study, we evaluated the function of TFA in the mitochondria apoptotic pathway using mathematical modeling. We found that TFA-enhanced B-cell lymphoma 2 (Bcl-2) overexpression can theoretically give rise to bistability. The bistability is highly robust against parametric stochasticity while also conferring considerable variability in survival threshold. Stochastic simulations faithfully match the TFA dose response pattern seen in experimental studies. In addition, we identified a dose- and time-dependent synergy between TFA and nimodipine, a clinically used neuro-protective drug. This synergistic effect was enhanced by bistability independent of temporal factors. Precise application of pulsed doses of TFA can also promote survival compared with sustained TFA treatment. These data collectively demonstrate that TFA treatment can give rise to bistability and that synergy between TFA and nimodipine may offer a promising strategy for developing therapeutic neuro-protection against ischemic stroke.