Effects of Environmental Stresses on Synthesis of 2-Phenylethanol and IAA by Enterobacter sp. CGMCC 5087.

2-Phenylethanol (2-PE) and indole-3-acetic acid (IAA) are important secondary metabolites produced by microorganisms, and their production are closely linked to the growth state of microorganisms and environmental factors. Enterobacter CGMCC 5087 can produce both 2-PE and IAA depending on α-ketoacid decarboxylase KDC4427. This study aimed to investigate the effects of different environment factors including osmotic pressure, temperature, and pH on the synthesis of 2-PE and IAA in Enterobacter sp. CGMCC 5087. The bacteria exhibited an enhanced capacity for 2-PE synthesis while not affecting IAA synthesis under 5% NaCl and pH 4.5 stress conditions. In an environment with pH 9.5, the synthesis capacity of 2-PE remained unchanged while the synthesis capacity of IAA decreased. The synthesis ability of 2-PE was enhanced with an increase in temperature within the range of 25 °C to 37 °C, while the synthesis capacity of IAA was not affected significantly. Additionally, the expression of KDC4427 varied under stress conditions. Under 5% NaCl stress and decreased temperature, expression of the KDC4427 gene was increased. However, altering pH did not result in significant differences in gene expression levels, while elevated temperature caused a decrease in gene expression. Furthermore, molecular docking and molecular dynamics simulations suggested that these conditions may induce fluctuation in the geometry shape of binding cavity, binding energy, and especially the dαC-C- value, which played key roles in affecting the enzyme activity. These results provide insights and strategies for the synthesis of metabolic products 2-PE and IAA in bacterial fermentation, even under unfavorable conditions.

Neuroprotective effect of licochalcone A against oxygen-glucose deprivation/reperfusion in rat primary cortical neurons by attenuating oxidative stress injury and inflammatory response via the SIRT1/Nrf2 pathway.

Perinatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of neonatal death and neurological disability. Oxidative stress and neuroinflammation are typical pathogenic factors of HIE. Licochalcone A (LCA) exerts various biological properties, including anti-inflammatory and antioxidant activities. However, no data have been reported to elucidate the role of LCA in the development of HIE. In the present study, primary cultured rat cortical neurons were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro to simulate the in vivo situation of neonatal HIE. Interestingly, LCA significantly antagonized cell injury under OGD/R by increasing cell survival, inhibiting lactate dehydrogenase (LDH) release and cell apoptosis. Furthermore, treatment with LCA suppressed oxidative stress by decreasing reactive oxygen species (ROS) production and malondialdehyde (MDA) content, and increasing superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in primary rat cortical neurons after OGD/R. LCA stimulation also restrained OGD/R-triggered increase in pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production. Importantly, LCA treatment effectively counteracts OGD/R-mediated downregulation of silent information regulator 1 (SIRT1), nuclear factor erythroid2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1), and upregulation of nuclear factor kappa B p65 (NF-κB p65). Moreover, administration with SIRT1 inhibitor EX527 partly abolished LCA-induced neuroprotective effects on rat cortical neurons exposed to OGD/R. In conclusion, our study indicates that LCA exerts a neuroprotective effect against OGD/R-induced neuronal injury in rat primary cortical neurons, suggesting that LCA might act as a candidate therapeutic target drug used for HIE and related diseases.

[Protective effects of curcumin on neonatal rats with necrotizing enterocolitis].

OBJECTIVE: This study examined the effects of curcumin on intestinal histopathological changes, cyclooxygenase-2 (COX-2) expression, and tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) concentrations in neonatal rats with necrotizing enterocolitis (NEC), in order to investigate the effects of curcumin against NEC. METHODS: Forty neonatal rats were randomly divided into four groups (n=10 each): normal control, solvent control, NEC model, and curcumin intervention. The general situations of rats were observed for 3 consecutive days, and the rats were then sacrificed on the 4th day. Intestinal tissues were obtained for examining the histopathological changes, COX-2 expression, and TNF-alpha and IL-10 concentrations. RESULTS: Curcumin treatment ameliorated the general situations and histopathological signs in rats with NEC. TNF-alpha and IL-10 concentrations in the NEC model and the curcumin intervention groups increased significantly compared with those in the normal and solvent control groups (p<0.05). The concentration of TNF-alpha decreased (p<0.05), while the concentration of IL-10 increased significantly in the curcumin intervention group in comparison with the NEC model group (p<0.05). Immunohistochemistry results indicated that the positive expression of COX-2 in the curcumin intervention group was significantly lower than that in the NEC model group. CONCLUSIONS: Curcumin has protective effects against NEC in neonatal rats, possibly through inhibiting COX-2 expression, reducing TNF-alpha content, and increasing IL-10 content.