Resveratrol (Res) is a natural compound that possesses anti-inflammatory properties. However, the protective molecular mechanisms of Res against lipopolysaccharide (LPS)-induced inflammation have not been fully studied. In the present study, RAW264.7 cells were stimulated with LPS in the presence or absence of Res, and the subsequent modifications to the LPS-induced signaling pathways caused by Res treatment were examined. It was identified that Res decreased the mRNA levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response protein MyD88, TIR domain-containing adapter molecule 2, which suggested that Res may inhibit the activation of the TLR4 signaling pathway. It suppressed the expression levels of total and phosphorylated TLR4, NF-κB inhibitor, p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2 and interferon (IFN) regulatory factor 3 (IRF3) proteins. Following treatment with Res or specific inhibitors, the production of pro-inflammatory mediators including tumor necrosis factor-α, interleukin (IL)-6, IL-8 and IFN-β were decreased and the expression of anti-inflammatory mediator IL-10 was increased. These results suggested that Res may inhibit the signaling cascades of NF-κB, MAPKs and IRF3, which modulate pro-inflammatory cytokines. In conclusion, Res exhibited a therapeutic effect on LPS-induced inflammation through suppression of the TLR4-NF-κB/MAPKs/IRF3 signaling cascades.

Pseudorabies virus (PRV) is one of the most important pathogens of swine, resulting in devastating disease and economic losses worldwide. Nevertheless, there are currently no antiviral drugs available for PRV infection. Resveratrol (Res) was identified to exert its antiviral activity by inhibiting the PRV replication in preliminary investigations. In our previous study, we found that Res has anti-PRV activity in vitro. Here, we show that Res can effectively reduce the mortality and increase the growth performance of PRV-infected piglets. After Res treatment, the viral loads significantly (p < 0.001) decreased. Pathological symptoms, particularly inflammation in the brain caused by PRV infection, were significantly (p < 0.001) relieved by the effects of Res. In Res-treated groups, higher levels of cytokines in serum, including interferon gama, interleukin 12, tumor necrosis factor-alpha and interferon alpha were observed at 7 days post infection. These results indicated that Res possesses potent inhibitory activity against PRV-infection through inhibiting viral reproduction, alleviating PRV-induced inflammation and enhancing animal immunity, suggesting that Res is expected to be a new alternative control measure for PRV infection.

This study was aimed to evaluate the effect of tannic acid (TA), a natural plant polyphenol astringent, on wound healing in vitro and in vivo, and to elucidate the underlying molecular signaling pathway in the wound healing. Approach: Cutaneous skin wounds were created in rats and then treated until closure with purified TA, serum or tissue samples were collected to test the concentration of factors by enzyme-linked immunosorbent assay (ELISA), and the expression in gene or protein was measured by quantitative real-time polymerase chain reaction or Western blot. We explored the cell-/dose-specific responses of TA (0.1-0.4 lg/mL) on proliferation and gene and protein expression of fibroblast NIH 3T3 cells. Results: The wounds on rats treated by TA got healed faster than those in the untreated group. The histopathology study showed that TA accelerated reepithelialization and increase in hair follicles could be detected. The levels of growth factors including basic fibroblast growth factor (bFGF), transforming growth factor-beta, and vascular endothelial growth factor in TA-treated groups were all increased, and the content of interleukin-1 (IL-1) and IL-6 was decreased significantly when compared with that of the untreated group. The NIH 3T3 cells grow faster in 6 h at concentration of 0.1 lg/mL, and the expression of bFGF in gene and protein was increased significantly in the 0.1 lg/mL TA group. Further study revealed that the protein levels of bFGF, extracellular signal regulated kinase (Erk) 1/2, and P-Erk 1/2 in Erk 1/2 pathway were increased after TA treatment. Innovation: The role of TA in wound healing efficacy is unclear; this study, therefore, assesses the effects of TA on wound healing in different periods and the underlying molecular mechanisms. Conclusion: These results suggested that TA could accelerate wound healing through modulation of inflammatory cytokines and growth factors and activate Erk 1/2 pathway. In conclusion, TA may be a potential agent in promoting wound healing.

Over the past decade, oxidative stress was shown to be a key factor for various diseases. The term “antioxidant” also rapidly gained attention worldwide, viewed as beneficial in disease prevention. Resveratrol (RSV), a natural polyphenol, is a plant antitoxin formed in response to harmful environmental factors such as infection and injury. This antitoxin is found in grapes, strawberries, peanuts, or herbal medicines and exhibits many pharmacological effects involved in antitumor, anti-inflammatory, antiaging, and antioxidation stress mechanisms. Recently, numerous in vitro and in vivo experiments have shown that RSV harbors antioxidative stress properties and can be used as an antioxidant. Here, we review the free radical scavenging ability, antioxidant properties, signaling pathways, expression and regulation of antioxidant enzymes, and oxidative stress-related diseases associated with RSV.

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