A traditional Chinese tea with many pharmacological effects, vine tea (VT) is considered a potential dietary supplement to improve type 2 diabetes (T2D). To investigate the effect and mechanism of VT on glucose and lipid metabolic disorders in T2D rats, Wistar rats fed a normal diet served as the normal control, while rats fed a high-fat diet combined with low-dose streptozotocin (STZ)-induced T2D were divided into three groups: The model group (MOD); the positive control group (MET, metformin at 200 mg/kg/d); and the VT-treated group (VT500, allowed to freely drink 500 mg/L VT). After four weeks of intervention, biochemical metrics indicated that VT significantly ameliorated hyperglycemia, hyperlipidemia and hyperinsulinemia in T2D rats. Metabolomics research indicated that VT regulated the levels of metabolites closely related to glucose and lipid metabolism and promoted glycogen synthesis. Furthermore, VT had a significant influence on the expression of key genes involved in the Akt signaling pathway, inhibited gluconeogenesis through the Akt/Foxo1/Pck2 signaling pathway, and reduced fatty acid synthesis via the SREBP1c/Fasn signaling pathways. In conclusion, VT has great potential as a dietary supplement to ameliorate glucose and lipid metabolic disorders via the Akt signaling pathway in T2D rats.

Ischemia-reperfusion injury is a leading cause of acute kidney injury (AKI), which is characterized by high morbidity and mortality, as well as a substantial risk of progression to chronic kidney disease (CKD). Although supportive care has improved considerably, effective disease-modifying therapies are still lacking. Therefore, the development of new therapeutic drugs for ischemic AKI is crucial. Active metabolites derived from medicinal plants, owing to their low toxicity and multi-target characteristics, are promising candidates for ischemic AKI therapy. This study reviews the pathogenesis of ischemic AKI from multiple dimensions, including metabolic disturbances, oxidative stress, inflammation, endoplasmic reticulum stress, mitochondrial dysfunction, and several forms of regulated cell death (e.g., ferroptosis, apoptosis, pyroptosis). It also summarizes plant metabolites (polyphenols, phenylpropanoids, terpenoids, saponins, alkaloids, and extracts) that can ameliorate ischemic AKI by targeting the aforementioned mechanisms. These metabolites exert their protective effects by modulating key signaling pathways (e.g., Nrf2/HO-1, NF-κB, PI3K/Akt). However, further mechanistic studies, standardization, and well-designed clinical trials are essential for their use and to ensure their integration into clinical practice as effective therapeutic options.