Tea polyphenols (TPP) as a promising wound healing agent: TPP exerts multiple and distinct mechanisms at different phases of wound healing in a mouse model.

Polyphenols have been widely used to treat various chronic skin diseases because they are beneficial in wound healing and show anti-inflammatory effects, however, the mechanism of action remains ambiguous. Previously, we reported the wound healing capability of tea polyphenols (TPP), the major functional component of tea, in vivo. The current study aimed to address the mechanisms of TPP in wound healing during different phases (inflammation, proliferation and remodeling). During the inflammation phase, TPP reduced the production of proinflammatory cytokines (IL-1ß, IL-6 and TNF-α) and inhibited infiltration of neutrophils; during the proliferation phase, TPP promoted the expression of growth factor VEGF-A, which can promote vascular endothelial cell division and induce angiogenesis; TPP improved the morphology of the wound and restored the ratio of type III/I collagens during the remodeling phase, as determined by Masson-trichrome staining and Sirius red staining assays. By tracking the changes in the wound area, TPP and recombinant human epidermal growth factor (rhEGF), rather than povidone-iodine (PVP-I), were able to promote wound healing. These results suggest that TPP plays a pivotal role in all the key stages of wound healing and displays distinct mechanisms from rhEGF, suggesting clinical significance for the future application of TPP as a natural wound healing agent.

Transcriptome analysis provides insight into the anti-diabetic mechanism of theaflavins in high-fat diet and streptozotocin-induced mice.

Black tea exhibits potential to improve hyperglycemia and insulin resistance, where theaflavins (TFs) are its characteristic components. The aim of this study was to explore the anti-diabetic mechanism of TFs. High-fat diet and streptozotocin-induced type 2 diabetes (T2D) mice were administered with TFs by gavage daily for 5 weeks. The biochemical analysis suggested that TFs possess potential anti-diabetic activity, which is comparable to that of metformin. RNA-sequencing analysis showed that TFs had a significant influence on the hepatic transcriptional profile of the T2D mice. The nine significantly enriched KEGG pathways were mainly associated with pancreatic secretion, digestion and metabolism of fat, protein and glycerolipid, and tight junctions. Quantitative real-time PCR and immunohistochemistry analysis verified that TFs improved pancreas function and intestine tight junction, with an increase in the expression of carboxyl ester lipase (Cel), chymotrypsinogen B (Ctrb1), pancreatic triglyceride lipase (Pnlip) and chymotrypsin-like elastase 3B (Cela3b) in the pancreas and cingulin and claudin-1 in the intestine. TFs improved mitochondrial biogenesis with the downregulation of peroxisome proliferator-activated receptor coactivator (PGC) 1α and 1ß in the liver, but had less effect on the muscle. This work revealed the comprehensive mechanism of TFs against T2D, suggesting that TFs are a potential natural agent for improving type 2 diabetes.

Tea Polyphenols Attenuates Inflammation via Reducing Lipopolysaccharides Level and Inhibiting TLR4/NF-κB Pathway in Obese Mice.

Obesity is a worldwide epidemic and increases the risk of metabolic syndrome through chronic inflammation. Tea polyphenols (TP), the major functional component of tea, has shown preventive effects on obesity and obesity-related disease, but the underlying mechanism is complicated and remains obscure. The present study was aimed to elucidate the anti-inflammation effect of TP in high-fat-diet (HFD)-induced obese mice. Results showed that TP reduced obesity-induced inflammation and systemic lipopolysaccharides (LPS) level. The decrease of LPS level in circulation was followed by the downregulation of LPS specific receptor, toll-like receptor 4 (TLR4), and its co-receptor cluster of differentiation 14 (CD14) and adaptor protein differentiation factor 88 (MyD88) in hepatic and adipose tissues. That further inhibited the activation of nuclear factor κB (NF-κB). The serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1ß) and interleukin-6 (IL-6) were significantly decreased by TP in HFD-fed mice. TP also maintained the intestinal barrier integrity by increasing intestinal tight junction proteins and reversed gut dysbiosis in obese mice. These results suggested that TP attenuated obesity-induced inflammation by reducing systemic LPS level and inhibiting LPS-activated TLR4/NF-κB pathway.