Wenxin Granule Ameliorates Hypoxia/Reoxygenation-Induced Oxidative Stress in Mitochondria via the PKC-δ/NOX2/ROS Pathway in H9c2 Cells.

Myocardial infarction and following reperfusion therapy-induced myocardial ischemia/reperfusion (I/R) injury have been recognized as an important subject of cardiovascular disease with high mortality. As the antiarrhythmic agent, Wenxin Granule (WXG) is widely used to arrhythmia and heart failure. In our pilot study, we found the antioxidative potential of WXG in the treatment of myocardial I/R. This study is aimed at investigating whether WXG could treat cardiomyocyte hypoxia/reoxygenation (H/R) injury by inhibiting oxidative stress in mitochondria. The H9c2 cardiomyocyte cell line was subject to H/R stimuli to mimic I/R injury in vitro. WXG was added to the culture medium 24 h before H/R exposing as pretreatment. Protein kinase C-δ (PKC-δ) inhibitor rottlerin or PKC-δ lentivirus vectors were conducted on H9c2 cells to downregulate or overexpress PKC-δ protein. Then, the cell viability, oxidative stress levels, intracellular and mitochondrial ROS levels, mitochondrial function, and apoptosis index were analyzed. In addition, PKC-δ protein expression in each group was verified by western blot analysis. Compared with the control group, the PKC-δ protein level was significantly increased in the H/R group, which was remarkably improved by WXG or rottlerin. PKC-δ lentivirus vector-mediated PKC-δ overexpression was not reduced by WXG. WXG significantly improved H/R-induced cell injury, lower levels of SOD and GSH/GSSG ratio, higher levels of MDA, intracellular and mitochondrial ROS content, mitochondrial membrane potential and ATP loss, mitochondrial permeability transition pore opening, NOX2 activation, cytochrome C release, Bax/Bcl-2 ratio and cleaved caspase-3 increasing, and cell apoptosis. Similar findings were obtained from rottlerin treatment. However, the protective effects of WXG were abolished by PKC-δ overexpression, indicating that PKC-δ was a potential target of WXG treatment. Our findings demonstrated a novel mechanism by which WXG attenuated oxidative stress and mitochondrial dysfunction of H9c2 cells induced by H/R stimulation via inhibitory regulation of PKC-δ/NOX2/ROS signaling.

Characteristics of nitrogen and phosphorus adsorption by Mg-loaded biochar from different feedstocks.

Herein, biochars from 6 different feedstocks (taro straw, corn straw, cassava straw, Chinese fir straw, banana straw, and Camellia oleifera shell) were produced using magnesium chloride (MgCl2) as a modifier due to their sorption behavior toward NH4+-N and phosphorus in an aqueous solution. The biochar characteristics were evaluated, including pH, pHPZC, biochar magnesium content, and total pore volume (PVtot). The experimental results in terms of the kinetics and equilibrium isotherms showed that the cassava straw and banana straw biochars exhibited the theoretical maximum saturated adsorption capacities of 24.04 mg·g-1 (NH4+-N) and 31.15 mg·g-1 (TP), respectively. Biochar produced from these feedstocks had higher magnesium contents and greater total pore volumes, reflecting the significant contributions from magnesium and steric effects. FTIR, XRD, and SEM/EDS analyses demonstrated that NH4+-N and TP sorption mechanisms predominantly involved surface electrostatic attraction, Mg2+ precipitates and complexation with surface hydroxyl functional groups.

Angelica sinensis reduced Aß-induced memory impairment in rats.

BACKGROUND: Studies have shown that Angelica sinensis (JiLin AoDong Medicine Industry Groups Co., Ltd., Jilin, China) root (AS) ameliorates various diseases, although its effects in Alzheimer's disease (AD) have not been elucidated. PURPOSE: The present study examined the effects of AS in a rat model of AD. METHODS: Positional Aß injections were administered to rats. The behavioral effects of AS administration were examined using the Morris water maze, and the molecular effects on gene and protein expression, and apoptosis, were determined. RESULTS: AS reversed the social behavioral impairments observed in this rat model of Aß-induced memory impairment. Western blot analysis also revealed lower hippocampal levels of Aß and ß-site amyloid precursor protein-cleaving enzyme. Terminal deoxynucleotidyl transferased UTP nick end labeling indicated that AS significantly inhibited apoptosis via effects on nuclear factor kappa B (NF-κB) signaling. Real-time PCR, enzyme-linked immunosorbent assay, and immunohistochemical staining indicated that AS effectively inhibited inflammation and upregulated expression of glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) in the hippocampus of this rat AD model. DISCUSSION: AS effectively rescued the symptoms of AD in a rat model by inhibiting inflammation, apoptosis, and NF-κB signaling pathway. CONCLUSION: These findings suggested that AS could provide a potential drug for the treatment of AD.