It has been demonstrated in some studies that triterpenoid acid extract fromEriobotrya japonica leaf is beneficial to prevent hyperlipidemia or insulin resistance. However, the effect of triterpenoid acids in Eriobotrya japonica leaf on a series of typical symptoms of metabolic syndrome (MetS) has been rarely studied systematically. Therefore, the present study aims to systematically evaluate the effect of Eriobotrya japonica leaf triterpenoid acids (ELTA) on MetS and explore its potential mechanism. ELTA (HPLC purity 95.2 %) was prepared and administered orally (200 mg/kg) to C57BL/6 J mice fed with a high-fat diet (HFD) for 12 weeks. Pioglitazone (30 mg/kg) was used as a positive control drug. Food intake, body weight, total lipid in feces, lipid profiles, inflammatory factors in serum, hepatic glutathione, and lipid peroxide were measured. Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed to evaluate insulin sensitivity. RT-qPCR and molecular docking were performed to explore the potential mechanism. ELTA administration reduced body weight gain, relative liver weight, and relative visceral adipose weight. The levels of serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, hepatic total cholesterol, and hepatic triglycerides were also reduced. ELTA reduced the area under curve (AUC) of blood glucose curves in OGTT and ITT. Relative mRNA level analysis of genes related to MetS showed that ELTA can effectively increase the transcriptional levels of Nrf2, HO-1, PPAR-γ, GluT2, GK, FXR, while effectively decrease those of PTP1B, p65, TNF-α, IL-6, SREBP, 11βHSD-1. Molecular docking showed that the ligands in ELTA can bind to 11βHSD-1, GK, PPAR-γ, and JNK, the important targets involved in MetS. ELTA can effectively alleviate visceral central obesity, insulin resistance, dyslipidemia, oxidative stress, and inflammation of HFD-induced MetS in C57BL/6 J mice. This is possibly achieved by acting on 11βHSD-1, GK, PPAR-γ, and JNK.

The interest focusing on Eriobotrya japonica leaf triterpene acid (ELTA) has increased recently because of its beneficial effects on health. However, there has been a lack of experimental data on its toxicity. The present study therefore was conducted to evaluate its toxicity in ICR mice. The results showed that ELTA produced neither mortality nor toxicity of the main organs in ICR male and female mice in both acute (0.30, 0.65, 1.39, and 3.00 g·kg⁻¹ body weight) and subacute (150, 300, and 600 mg·kg⁻¹ BW) 28‐day toxicity studies. Because of lacking apparently adverse effects found in the hematology, clinical biochemistry, and histopathology evaluation, results of the present study together with the beneficial effects make ELTA as a promising dietary supplement and indicated that ELTA administered orally might have a large safety margin for human.

In an aqueous buffer system, serious reverse and side reactions were found in the asymmetric reduction of 2-octanone with Saccharomyces cerevisiae. However, some nonionic surfactants added to the aqueous buffer system improved the bioreduction process by decreasing the reverse and side reaction rates in addition to effectively increasing the average positive reaction rate. Further, a shorter carbon chain length of hydrophilic or hydrophobic moieties in surfactants resulted in a higher yield of (S)-2-octanol. The alkylphenol ethoxylate surfactants had a less influence than polyoxyethylenesorbitan trialiphatic surfactants on the product e.e. It suggested that the product e.e. resulting from the change of carbon chain length of the hydrophobic moieties varied markedly compared with the change of carbon chain length of the hydrophilic moiety. Emulsifier OP-10 and Tween 20 markedly enhanced the yield and product e.e. at the concentration of 0.4 mmol L−1 with a yield of 73.3 and 93.2%, and the product e.e. of 99.2 and 99.3%, respectively, at the reaction time of 96 h.

Oleanolic acid (OA) exhibits pronounced neuroprotective effects in the central nervous system; however, its clinical translation is limited by poor solubility and low bioavailability. To overcome these limitations, we developed glutathione-PEGylated OA liposomes (GSH-PEG-OA-LIP) via a post-insertion method, achieving an load efficiency of 94.2%. In vivo imaging demonstrated that GSH-PEG modification significantly prolonged blood circulation and enhanced brain accumulation compared to unmodified liposomes. In a mouse model of scopolamine (SCOP)-induced cognitive deficit, GSH-PEG-OA-LIP treatment effectively reversed short- and long-term memory impairments. Biochemical analyses revealed that the treatment restored hippocampal cholinergic function by increasing acetylcholine (ACh) levels and choline acetyltransferase (ChAT) activity, while simultaneously alleviating oxidative stress through reduced malondialdehyde (MDA) content and increased superoxide dismutase (SOD) activity. Furthermore, molecular docking and molecular dynamics simulations confirmed stable interactions between OA and key signaling targets—specifically PKC, PI3Kγ, MEK, and IP3R—suggesting a multi-targeted mechanism of action. Collectively, these results highlight GSH-PEG-OA-LIP as an efficient brain-targeted delivery system and a promising therapeutic strategy for cognitive disorders.