Background: Tartary buckwheat bran is an important natural source of quercetin and isoquercetin. Quercetin and isoquercetin are both powerful α-glucosidase inhibitors. Although the IC₅₀ of isoquercetin as α-glucosidase inhibitor was much higher than that of quercetin, the bioavailability of isoquercetin was higher than that of quercetin. Hence, we are interested in the antidiabetic effect of isoquercetin in diabetic KK -A^y mice. Methods: The hypoglycemic effect of isoquercetin in a type 2 diabetic animal model (KK-A^y mice) was studied. Isoquercetin was administrated at doses of 50, 100 and 200 mg/kg for 35 days. Results: It was found that fasting blood glucose concentration was decreased with the 200 mg/kg group (p < 0.01) the most efficient compared with the diabetic control group. In addition, there was significant decrease in plasma C-peptide, triglyceride, total cholesterol and blood urea nitrogen levels after 35 days. Meanwhile, glucose tolerance was improved, and the immunoreactive of pancreatic islets β-cells was promoted. Conclusions: These results suggest that isoquercetin had a regulative role in blood glucose level and lipids, and improved the function of pancreatic islets. Isoquercetin may be useful in the treatment of type 2 diabetes mellitus.

Although previous studies have reported that saponins (ginsenosides, the major active and most representative ingredients in Panax ginseng C.A. Meyer) exerted a good ameliorative effect on cisplatin (CP)-induced acute kidney injury in animal models, little attention has been paid to a large number of polysaccharides isolated and purified from ginseng. This work aimed to investigate the protective effect and the possible molecular mechanism of ginseng polysaccharide (WGP) on CP-induced kidney toxicology in mice. The results from biomarker analysis including serum creatinine (CRE) and blood urea nitrogen (BUN) confirmed the protective effect of WGP at 200 and 400 mg/kg on CP-induced renal-toxicology. We found that WGP reduces the apoptosis of kidney cells by inhibiting endoplasmic reticulum (ER) stress caused by CP, which is manifested by increased phosphorylation of PERK. In addition, the apoptosis-associated with caspase 3 activation in renal cells induced by CP was inhibited after administration of WGP, and the phosphorylation levels of PI3K and AKT were also reduced significantly. We also demonstrated that after exposure to CP, the unfolded protein response signaling pathway PERK-eIF2α-ATF4 axis was significantly activated, manifested by increased phosphorylation of eIF2α and increased expression of ATF4 and CHOP. Interestingly, the WGP administration improves this situation. Furthermore, the supplement of WGP inhibited the overexpression of nuclear factor-kappa B p65 (NF-κB p65) and tumor necrosis factor-α (TNF-α) caused by CP exposure. In short, for the first time, our findings indicated that WGP could effectively prevent CP-induced ER stress, inflammation, and apoptosis in renal cells, in part, by regulating the PI3K/AKT and PERK-eIF2α-ATF4 signaling pathways.

The excessive employment of acetaminophen (APAP) is capable of generating oxidative stress and apoptosis, which ultimately result in acute liver injury (ALI). Ganoderma lucidum polysaccharides (GLPs) exhibit hepatoprotective activity, yet the protective impact and potential mechanism of GLPs in relation to APAP-induced ALI remain ambiguous. The intention of this research was to scrutinize the effect of GLPs on APAP-induced ALI and to shed light on their potential mechanism. The results demonstrated that GLPs were capable of notably alleviating the oxidative stress triggered by APAP, as shown through a significant drop in the liver index, the activities of serum ALT and AST, and the amounts of ROS and MDA in liver tissue, along with an increase in the levels of SOD, GSH, and GSH-Px. Within these, the hepatoprotective activity at the high dose was the most conspicuous, and its therapeutic efficacy surpassed that of the positive drug (bifendate). The results of histopathological staining (HE) and apoptosis staining (TUNEL) indicated that GLPs could remarkably inhibit the necrosis of hepatocytes, the permeation of inflammatory cells, and the occurrence of apoptosis induced by APAP. Moreover, Western blot analysis manifested that GLPs enhanced the manifestation of Nrf2 and its subsequent HO-1, GCLC, and NQO1 proteins within the Nrf2 pathway. The results of qPCR also indicated that GLPs augmented the expression of antioxidant genes Nrf2, HO-1, GCLC, and NQO1. The results reveal that GLPs are able to set off the Nrf2 signaling path and attenuate ALI-related oxidative stress and apoptosis, which is a potential natural medicine for the therapy of APAP-induced liver injury.

This study focused on developing Panos nanoemulsion (P-NE) and enhancing the anti-inflammatory efficacy for the treatment of inflammation. The effects of P-NE were evaluated in terms of Nitric oxide (NO production) in Lipopolysaccharide (LPS), induced RAW 264.7 cells, Reactive oxygen species (ROS) generation using Human Keratinocyte cells (HaCaT), and quantitative polymerase chain reaction (qPCR) analysis. Sea buckthorn oil, Tween 80, and span 80 were used and optimize the process. Panos extract (P-Ext) was prepared using the fermentation process. Further high-energy ultra-sonication was used for the preparation of P-NE. The developed nanoemulsion (NE) was characterized using different analytical methods. Field emission transmission electron microscopy (FE-TEM) analyzed the spherical shape and morphology. In addition, stability was analyzed by Dynamic light scattering (DLS) analysis, where particle size was analyzed 83 nm, and Zeta potential −28.20 ± 2 (mV). Furthermore, 90 days of stability was tested using different temperatures conditions where excellent stability was observed. P-NE are non-toxic in (HaCaT), and RAW264.7 cells up to 100 µg/mL further showed effects on ROS and NO production of the cells at 50 µg/mL. The qPCR analysis demonstrated the suppression of pro-inflammatory mediators for (Cox 2, IL-6, IL-1β, and TNF-α, NF-κB, Ikkα, and iNOS) gene expression. The prepared NE exhibited anti-inflammatory effects, demonstrating its potential as a safe and non-toxic nanomedicine.

Damping-off disease caused by Rhizoctonia solani is a devastating soilborne disease that poses a serious threat to sustainable ginseng (Panax ginseng) production. In an effort to develop environmentally friendly control alternatives, we investigated the volatile constituents of Asarum heterotropoides essential oil using GC-MS in 2023 and identified methyleugenol as the predominant bioactive component, accounting for 21.32% of the total volatile fraction. Mycelial growth rate assays demonstrated that methyleugenol exerted pronounced antifungal activity against R. solani, with EC₅₀ and EC₉₀ values of 60 mg/L and 800 mg/L, respectively. Treatment at 0.1 mg/mL resulted in 51% growth inhibition after 4 days of incubation. To elucidate the underlying mechanisms of action, R. solani mycelia exposed to 0.1 mg/mL methyleugenol were harvested at 4 and 6 days post-treatment for integrated transcriptomic and untargeted metabolomic profiling. Transcriptome analysis revealed 1444 and 1157 significantly downregulated genes at 4 and 6 days, respectively, with 836 genes consistently repressed at both time points. GO and KEGG enrichment analyses indicated that these persistently suppressed genes were predominantly associated with protein processing in the endoplasmic reticulum, protein export, tyrosine metabolism, and peroxisome biogenesis. Metabolomic profiling identified 95 differentially accumulated metabolites that were commonly reduced across both time points, with KEGG pathway enrichment highlighting significant suppression of starch and sucrose metabolism and galactose metabolism pathways central to carbon source utilization. Integrative transcriptome–metabolome correlation analysis further uncovered three key transcription factors (gene-RDB_LOCUS74145, gene-RDB_LOCUS26344, and gene-RDB_LOCUS52181) implicated in the regulation of carbohydrate metabolism and tricarboxylic acid cycle-related metabolite production. Collectively, our findings indicate that methyleugenol suppresses R. solani growth through a multi-target mechanism involving impairment of carbon source metabolism, disruption of protein processing and secretion, and attenuation of cellular energy supply. These results provide a mechanistic foundation for the development of botanical fungicide-based strategies for the green management of ginseng damping-off disease.