Herbal tea with antioxidant ingredients has gained increasing attention in the field of functional foods due to their amelioration potential in aging‐related diseases. Wanglaoji herbal tea (WHT) is a kind of traditional beverage made from herbal materials. This study was performed to investigate its antioxidant activity and identify its protective effect on a H₂O₂‐induced cell damage model. In this study, we identified six kinds of phenolic acids with antioxidant activity in WHT, among which rosmarinic acid had the highest content and the highest contribution ratio to the antioxidant activity of WHT. Moreover, compared with the H₂O₂‐induced damage group, the WHT treatment group can significantly increase the viability of cells and decrease the ratio of senescence‐associated β‐galactosidase‐positive cells, intracellular malondialdehyde levels, and the percentage of G1 phase. Furthermore, enrichment analysis of differentially expressed genes revealed that heme oxygenase1 (HMOX1) was a key gene for protective effect of WHT on oxidative stress‐induced cell damage. Thus, WHT exerted protective effects not only by scavenging reactive oxygen species but also by inducing the expression of cytoprotective genes by activating the HMOX1 pathway, which showed that WHT had a potential of promoting health by reducing oxidative stress‐induced cell damage.

Monascus red (MR) is widely used as a natural food colorant and preservative in East Asia. However, the potential effects of MR during pregnancy remains unknown. In this study, MR was administrated to Sprague-Dawley (SD) rats at doses of 0, 0.50, 1.58, and 5.00 g/kg bw on gestational days 6-15 by oral gavage. In the maternal and embryo-fetal examinations, there were no marked toxicities in terms of general clinical signs, body weight, food consumption, serum endocrine indices, organ weights, thyroid histopathology, examinations of uterine contents and fetuses. In the gut microbiota analysis, the 5.00 g/kg bw dose of MR decreased the α diversity and slightly changed their community structure at the genus level. Yet no marked toxicities in maternal animals or embryo-fetal development were observed. The no-observed-adverse-effect-level (NOAEL) of the maternal and developmental toxicity through oral exposure to MR was 5.00 g/kg bw, the highest dose tested in rats.

Purpose Eucommiae Cortex (Eucommia ulmoides Oliv., cortex) had possessed multiple curative effect since ancient time. Nevertheless, the mechanism of EC serves as anti-osteoporotic herb remains further investigated. Methods Cytotoxicity assay and osteogenesis assay were adopted to filtrate the TCMs and osteoporosis model rats of was utilized to verify the anti-osteoporosis ability of EC. Network pharmacology was used to investigate the potential mechanisms of the EC against osteoporosis. The database including TCMSP, BATMAN TCM and TCMID were utilized to obtain the active compounds of EC, and their potential targets were predicted by SwissTarget-Prediction. Osteoporosis related targets were found by OMIM, DisGeNET and Gene Cards databases. The target interaction network was analyzed by STRING, GO enrichment and KEGG pathway analysis were carried out by DAVID database. Results Results of in vitro and in vivo experiments illustrated that EC showed no cytotoxicity and exhibited anti osteoporosis effect. A total number of 19 active components and 124 osteoporosis related targets of the EC were selected. KEGG pathway enrichment from bioinformatics suggested that EC prevented osteoporosis through the HIF-1 signaling pathway and estrogen signaling pathway, while results of RNA- sequencing suggesting HIF-1 signaling pathway. Moreover, genes Akt1, MAPK3 and EGFR may serve as the critical targets regulated by EC. Conclusion Our results showed that HIF-1 signaling pathway was vital pathway in EC against osteoporosis, with the participation of gene AkT1, MAPK3 and EGFR. Estrogen and VEGF signaling pathway were synergetic pathway of anti-osteoporosis

Titanium dioxide nanoparticles (nTiO₂) possess unique physicochemical properties, such as large specific surface area, enabling heavy metals adsorption like Cadmium (Cd), yet the combined risks to the ecosystem and human remain unclear. This 90-day study explored the combined effects of nTiO₂ (at a population-relevant dose of 100 mg/kg body weight administered via gavage) and cadmium chloride (CdCl₂) (50 mg Cd/L by drinking water) on kidney and gut microbiota of rats. Co-exposure of nTiO₂ and Cd significantly reduced the nephrotoxicity induced by Cd, with lower levels of urine biochemical indicators and Cd content, milder histopathological changes and ultrastructural damage. A two-way ANOVA analysis suggested antagonism between nTiO₂ and Cd on urinary creatinine (CRE) and Urea. Coincidentally, gut microbiota remained unaffected by nTiO₂ but was disrupted by Cd. Co-exposure also partially alleviated the adverse changes, restoring the decreased Beta-diversity and the relative abundance of bacteria to control levels. Furthermore, co-exposure resulted in a 19.2 % decline in the blood Cd concentration and an 8.6 % reduction in kidney, while the Cd content of 24 h feces was 3.6 % higher. These findings suggested antagonistic effects of nTiO₂ against Cd-induced nephrotoxicity and intestinal flora disorder in rats. The effects might be attributed to the adsorption of nTiO₂ on Cd, which resulted in the reduced Cd intake and distribution, coupled with increased excretion, thereby decreasing the Cd bioavailability. This study provides new evidence for understanding the impacts of nTiO₂ and Cd on mammals and will contribute to the further risk assessments of co-exposure to human health and environment safety.