Quercus infectoria Olivier (Fagaceae) nutgall, a traditional Asian medicine, is renowned for its efficacy in treating wounds and skin disorders. Although the gall extract has shown promising results in accelerating wound healing in diabetic animal models, its mechanisms, particularly the effects on redox balance, remain poorly understood. This study aims to investigate the effects and mechanisms of Q. infectoria gall ethanolic extract (QIG) on wound healing in fibroblasts, with a specific emphasis on its modulation of oxidative stress. Hydrogen peroxide (H₂O₂)-treated L929 cells were used as an in vitro model of oxidation-damaged fibroblasts. QIG exhibited potent antioxidant activity with 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS), and ferric reducing antioxidant power (FRAP) assay values of 305.43 ± 7.48, 508.94 ± 15.12, and 442.08 ± 9.41 µM Trolox equivalents (TE)/µg, respectively. Elevated H₂O₂ levels significantly reduced L929 cell viability, with a 50% lethal concentration of 1.03 mM. QIG mitigated H₂O₂-induced cytotoxicity in a dose-dependent manner, showing protective effects in pre-, post-, and co-treatment scenarios. QIG significantly reduced H₂O₂-induced intracellular reactive oxygen species production and inflammation-related gene expression (p < 0.05). Additionally, at 25 µg/mL, QIG remarkably improved wound closure in H₂O₂-treated L929 cells by approximately 9.4 times compared with the H₂O₂ treatment alone (p < 0.05). These findings suggest QIG has potential therapeutic applications in wound healing, mediated through the regulation of oxidative stress and inflammatory response.

Background: Banana inflorescence is one of the edible parts of banana. It is well-known to have antioxidants and anti-diabetic potential health benefits. Methods: In this study, the banana inflorescence from Musa (ABB group) Namwa Mali-Ong was prepared using ethanol extraction and investigated for its biochemical compositions and biological activities. The 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging, ferric reducing antioxidant power (FRAP), and 2,2’-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) free radical scavenging activity assays were performed. The phytochemical composition of the extract was analyzed using the ultra-high-performance liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry (UHLC-ESI-QTOF/MS) technique. Additionally, the ability of the extract to stimulate glucose in C2C12 myotube was investigated. Results: The ethanolic extract of banana inflorescence contained carbohydrate, protein, phenolic, and flavonoid compounds. The results show that the extract exhibited low-level antioxidant activities. For example, the half-maximal inhibitory concentration (IC50) in the DPPH and ABTS assays was at 27.89 ± 0.054 and 21.33 ± 0.87 mg/mL, respectively. Although the extract possesses low-level antioxidant activities, it stimulated glucose uptake in C2C12 myotubes in a dose- and time-dependent fashion. Consistently, the LC-ESI-QTOF/MS analysis in both positive and negative electrospray ionization modes reveals several components in the extract such as phytosphingosine and α-linolenic acid that have previously been shown to exhibit an anti-diabetic activity.Conclusion: The results show that the inflorescence ethanolic extract possesses antioxidant and anti-diabetic activities and may potentially be developed into a health-promoting product such as an anti-diabetic drug. Keywords: antioxidant activity; banana inflorescence; glucose uptake; anti-diabetic; C2C12 myotubes

The dynamic ability of adipocytes in adipose tissue to store lipid in response to changes in the nutritional input and inflammatory elicitors has a major impact on human health. Previously, we established laminarin-coated beads or LCB as an inflammatory elicitor for adipocytes. However, it was not clear whether LCB inhibits lipid accumulation in adipocytes. Here, we show that LCB acts in the early stage of adipogenesis through both interleukin-1 receptor-associated kinases (IRAK) and spleen tyrosine kinase (SYK) pathways, resulting in the activation of the AMP-activated protein kinase (AMPK) and nuclear factor-κB (NF-κB) complexes, which subsequently cause cell cycle arrest, downregulation of the key transcription factors and enzymes responsible for adipogenesis, inhibition of adipogenesis, and stimulation of an inflammatory response. While LCB could effectively block lipid accumulation during the early stage of adipogenesis, it could stimulate an inflammatory response at any stage of differentiation. Additionally, our results raise a possibility that toll-like receptor 2 (TLR2) and C-type lectin domain family 7 member A (CLEC7A/Dectin-1) might be potential β-glucan receptors on the fat cells. Together, we present the mechanism of LCB, as fungal-like particles, that elicits an inflammatory response and inhibits adipogenesis at the early stage of differentiation.

Adipocytes from white-adipose tissue are known to produce inflammatory cytokines, which play a major role in energy balance and metabolism. While they can respond to pathogen-associated molecular pattern (PAMPs) such as lipopolysaccharide (LPS) from bacteria, it is not known whether adipocytes can be stimulated by fungal cells. Previously, adipocytes were shown to produce toll-like receptor 2 (TLR2), a β-glucan receptor, suggesting that they could respond to β-glucan on the fungal cell wall. In this study, we show that heat-killed yeast induce an inflammatory response in adipocytes. Using fungal-like particles, namely laminarin-coated beads (LCB), we find that these particles trigger the expression of many key inflammatory genes in dose- and time-dependent fashions in adipocytes. These results suggest that β-glucan on the fungal cell wall is sufficient to elicit an inflammatory response in adipocytes. In addition, we show that both LCB and LCB-treated conditioned medium from RAW 264.7 murine macrophages (LCB-RM) induce the expression of those inflammatory genes through IKKβ-IκBα proteins. Together, we conclude that the fungal-like particles and the conditioned medium elicit an inflammatory response in adipocytes through the canonical or classical NF-κB pathway.