Naringenin (NRG) is widely found in citrus fruits and has anti-inflammatory, hypoglycemic, and immunomodulatory effects. Previous studies have shown that NRG promotes gastrointestinal motility in mice constipation models, but there are few systematic evaluations of its effects on normal animals. This study first clarified the promotive effects of NRG on gastric emptying and small intestine propulsion (p < 0.01). NRG can also regulate the release of gastrointestinal hormones, including enhancing gastrin (GAS) and motilin (MTL) (p < 0.01), while reducing vasoactive intestinal peptide (VIP) secretion (p < 0.01). Using NRG to stimulate the isolated stomach, duodenum, and colon showed similar promotive effects to those observed in vivo (p < 0.01). A Western blot analysis indicated that this effect may be mediated by increasing the expression of stem cell factor (SCF) and its receptor (c-Kit) in these three segments, thus regulating their downstream pathways. It is worth noting that NRG can also increase the proportion of beneficial bacteria (Planococcaceae, Bacteroides acidifaciens, Clostridia_UCG-014) in the intestine and reduce the quantity of harmful bacteria (Staphylococcus). These findings provide a new basis for the application of NRG.

Mao Jian Green Tea flavonoids (MJGT_F) contain luteolin, luteolin-7-O-glucoside, eriodictyol, and eriodictyol-7-O-glucoside, among which the first three components have hypoglycemic effects; however, the overall hypoglycemic potential of MJGT_F remains unclear. This study demonstrated that MJGT_F inhibited α-glucosidase in vitro and improved metabolic parameters in a dose-dependent manner in T2DM (type 2 diabetes mellitus) rats (reducing blood glucose, triglyceride, total cholesterol, low-density lipoprotein, insulin, and the homeostatic model assessment of insulin resistance; increasing high-density lipoprotein, insulin sensitivity index, and glucagon-like peptide-1). High-dose MJGT_F (MJGT_F_H) showed optimal efficacy. Mechanistically, MJGT_F_H activated the AMPK pathway, evidenced by a significant increase in the p-AMPK/AMPK ratio and downregulation of hepatic gluconeogenic enzymes G6Pase and PEPCK. These coordinated effects collectively suggest enhanced hepatic glucose utilization and suppression of glucose overproduction. MJGT_F_H also modulated gut microbiota by enriching beneficial taxa (e.g., Akkermansia muciniphila, 11.17-fold vs. metformin) and reducing pathogens like Enterobacteriaceae. These findings highlight MJGT_F’s dual regulatory roles in glucose metabolism and microbiota, supporting its potential for diabetes management.

This study investigates the protective effects and underlying mechanisms of Mao Jian Black tea ethanol extract (MJBT_EE) on a mouse model of acute alcohol-induced liver injury (ALI). The animal model was established using the NIAAA method, and C57BL/6 mice were divided into the following groups: negative control group (NC), model control group (MG), silibinin positive control group (SL, 54 mg/kg), and MJBT_EE high- and low-dose groups (40 mg/mL, 20 mg/mL). The results showed that, compared to the MG, MJBT_EE significantly reduced serum levels of ALT, AST, TC, TG, LDL-C, TBIL, ALP and inflammatory cytokines IL-6, TNF-α, and IL-1β (p < 0.01), while upregulating HDL-C (p < 0.01). It also enhanced the activity of hepatic antioxidant enzymes SOD and GSH (p < 0.01) and reduced MDA content (p < 0.01). Further histopathological examination of liver tissue revealed that MJBT_EE_H markedly alleviated hepatocellular hydropic degeneration, swelling, and steatosis. The mechanism of action of MJBT_EE_H primarily involved activation of the PI3K/Akt pathway and suppression of excessive p-NF-κB activation. These findings indicate that Maojian black tea ethanol extract exerts significant protective effects against alcohol-induced liver injury, potentially through improving lipid metabolism, reducing oxidative stress and inflammatory responses, and modulating the PI3K/Akt/NF-κB signaling pathway.