Mechanisms of Antioxidant Dipeptides Enhancing Ethanol-Oxidation Cross-Stress Tolerance in Lager Yeast: Roles of the Cell Wall and Membrane.

High concentrations of ethanol could cause intracellular oxidative stress in yeast, which can lead to ethanol-oxidation cross-stress. Antioxidant dipeptides are effective in maintaining cell viability and stress tolerance under ethanol-oxidation cross-stress. In this study, we sought to elucidate how antioxidant dipeptides affect the yeast cell wall and membrane defense systems to enhance stress tolerance. Results showed that antioxidant dipeptide supplementation reduced cell leakage of nucleic acids and proteins by changing cell wall components under ethanol-oxidation cross-stress. Antioxidant dipeptides positively modulated the cell wall integrity pathway and up-regulated the expression of key genes. Antioxidant dipeptides also improved the cell membrane integrity by increasing the proportion of unsaturated fatty acids and regulating the expression of key fatty acid synthesis genes. Moreover, the addition of antioxidant dipeptides significantly (p < 0.05) increased the content of ergosterol. Ala-His (AH) supplementation caused the highest content of ergosterol, with an increase of 23.68 ± 0.01% compared to the control, followed by Phe-Cys (FC) and Thr-Tyr (TY). These results revealed that the improvement of the cell wall and membrane functions of antioxidant dipeptides was responsible for enhancing the ethanol-oxidation cross-stress tolerance of yeast.

Asprenols A-H, phenolic constituents from the stems of Ilex asprella.

Encouraged by the in vivo anti-inflammatory effect of aqueous extract of Ilex asprella stems, a further phytochemical investigation on I. asprella stems oriented by the in vitro NO production inhibition in RAW264.7 cells was conducted, which led to the isolation of eight new phenolic constituents, namely asprenols A-H (1-8), together with 12 known ones (9-20). The structures of the new compounds were established by extensive spectroscopic data analyses of HR-ESI-MS, IR, UV, and 1D and 2D NMR, and the absolute configurations were determined by comparison of experimental and calculated ECD analyses. All isolated were evaluated for the inhibition against NO production in RAW 264.7 cells, and several compounds showed moderate inhibitory effect.

Four new spirobenzylisoquinoline N-oxide alkaloids from the whole plant of Corydalis hendersonii.

Encouraged by the anti-myocardial ischemic effect of Corydalis hendersonii ethanol extract, a chemical reinvestigation of the whole plant of C. hendersonii was performed, which led to the isolation of four new spirobenzylisoquinoline N-oxide alkaloids, hendersines C-F (1-4), along with seven known isoquinoline alkaloids (5-11). The structures of the new isolates including absolute configurations were elucidated by the analysis of spectroscopic data and comparison of the experimental and calculated electronic circular dichroism (ECD) data. Compound 1 inhibited the NO production in lipopolysaccharide (LPS)-induced RAW 264.7 cells with an IC50 value of 70.3 µM, and increased the cell viabilities with 40.0 ±â€¯3.9% against the oxygen glucose deprivation injury in H9c2 cells at 40 µM.

Effects of liver depression and psychological stress on human uterine leiomyoma cells by an AR-cAMP-PKA signal transduction pathway.

OBJECTIVE: Based on the emotional theory of Traditional Chinese Medicine, and combined with the modern medicine theory of psychological stress, a research model of human uterine leiomyoma cells (ULM) was cultured in vitro to determine the effectiveness of adrenergic receptor (AR) agonists in human ULM cell growth. In addition, we studied the functional influence of "liver depression and psychological stress theory" on fibroid formation by intervening in the AR-cAMP-PKA signaling pathway. The intention was to establish a new method to prevent and cure fibroids through "liver depression and psychological stress theory" and provide an experimental basis for the Traditional Chinese Medicine emotional theory. MATERIALS AND METHODS: Primary human ULM cells were enriched by collagenase digestion. Immunohistochemistry and hematoxylin and eosin (HE) staining were used for cytological identification. Using this model, we studied intervention using specific AR agonists on ULM cells to observe the influence of "liver depression and psychological stress theory" on estrogen receptor (ER), progesterone receptor (PR), vascular endothelial growth factor (VEGF) and fibroblast growth factors (FGF). RESULTS: Norepinephrine (NE) and epinephrine (E) are adrenergic receptor agonists. They promoted ULM cell proliferation and increased the levels of ER, PR, VEGF and FGF. In contrast, isoproterenol (ISO) inhibited ULM cell proliferation and decreased the levels of ER, PR, VEGF and FGF. The protein expression of cAMP and PKA in ULM cells was reduced and the levels of ER, PR, VEGF and FGF were increased when co-treatment with the α-AR blocker (phentolamine). The ß-AR blocker (metoprolol) displayed an opposite effect. CONCLUSIONS: AR agonists modulated ER, PR, VEGF and FGF levels in ULM cells in an AR-cAMP-PKA-dependent signaling pathways to influence fibroid occurrence and development.