Soil bacterial community structure of mixed bamboo and broad-leaved forest based on tree crown width ratio.

Moso bamboo (Phyllostachysheterocycla (Carr.) Mitford cv. Pubescens) is an economically valuable plant in bamboo production areas of southern China, for which the management mode is crucial for improving the comprehensive benefits of bamboo forest stands. In this respect, mixed forested areas of bamboo and broad-leaved tree species can provide sound ecological management of bamboo in forestry operations. To further this goal, an outstanding question is to better understand the spatial distribution of soil bacterial communities in relation to the proportion of mixed in bamboo and broad-leaved forest. We analyzed soil bacterial community diversity and composition along a proportional gradient of 0-40% mixed-ratio (as represented by the width and size of the broad-leaved tree crown over the plot area) of bamboo and broad-leaved forest in Tianbao Yan Nature Reserve using the highthroughputsequencing of the 16S rRNA gene.Specifically, the sampling plots for the mixed proportions were divided according to the percentage of summed projected area of live broadleaf tree crowns. The main broad-leaved species in the five mixed ratio plots are the same. Each plot was 20 m × 20 m in size, and a total of 15 plots were established, three per forest ratio class. From each plot, soil samples were taken at the surface (0-10 cm depth) in December 2017. Our analysis revealed that soil bacterial diversity community structure and dominant flora changed under different mixing ratios of bamboo and broad-leaved trees. In the stand with a mixed ratio of 10-20%, the bacterial diversity index is higher; however, the diversity was lowest in the 20-30% stands. Among the 20-30% forest soil, Acidobacteria (Solibacteria, Solibacteriales, Acidobacteriales) was more abundant than in soils from other mixed-ratio stands.Redundancy analysis showed that mixed forest stand structure, soil pH, organic carbon, total nitrogen, and soil moisture all contributed to shaping the bacterial community structure. Changes in microbial communities were associated with species diversity in tree layers, availability of soil nutrients (SOC and TN), and changes in soil physical properties (MS, pH). Together, these empirical results suggest that different mixing ratios in the bamboo-broad-leaved mixed forest could influence the soil bacterial community structure indirectly, specifically by affecting the soil physical and chemical properties of the forest.

Effect of astragaloside IV against rat myocardial cell apoptosis induced by oxidative stress via mitochondrial ATP-sensitive potassium channels.

Astragaloside is one of the most common traditional Chinese medicines and is derived from Astragalus membranaceus. Astragaloside IV (AsIV) is a monomer located in an extract of astragaloside. The current study investigated the protective effects of AsIV against hydrogen peroxide (H2O2)-induced injury in cardiocytes and elucidated the mechanisms responsible for this protective effect. Cultured neonatal rat cardiocytes were divided into five experimental groups as follows: i) Dimethyl sulfoxide; ii) H2O2; iii) AsIV+H2O2; iv) AsIV+H2O2+5-hydroxydecanoate (5-HD); and v) nicorandil+H2O2. Cardiocyte survival was analyzed using an MTT assay. Lactate dehydrogenase (LDH) release was also assessed to evaluate the viability of the cells. Intracellular reactive oxygen species (ROS) were measured by 2,7-dichlorodihydrofluorescein diacetate staining. The apoptotic rate was measured by flow cytometry. Mitochondrial membrane potential (ΔΨm) and intracellular calcium were observed using a laser confocal microscopy system. The results indicated that AsIV promoted the survival of cardiocytes (P<0.05), attenuated LDH release (P<0.05), ROS production (P<0.01) and apoptosis (P<0.01), stabilized the ΔΨm and reduced intracellular calcium overload (P<0.01) compared with the H2O2 group. The mitochondrial adenosine triphosphate-sensitive potassium channel (mitoKATP) inhibitor 5-HD was observed to partially reverse the protective effect of AsIV. Following treatment with 5-HD, the survival of cardiocytes was reduced (P<0.05), LDH release (P<0.01) and ROS production (P<0.05) were stimulated, ΔΨm and intracellular calcium change were increased (P<0.01) and apoptosis was increased (P<0.01) compared with the AsIV+H2O2 group. Thus, AsIV has potential for use in the suppression of apoptosis resulting from H2O2 exposure, and mitoKATP activation may underlie this protective mechanism.

Compound K protects pancreatic islet cells against apoptosis through inhibition of the AMPK/JNK pathway in type 2 diabetic mice and in MIN6 ß-cells.

AIMS: Compound K (CK) is known to possess anti-diabetic activities but the mechanism for this action is unknown. The present study observed the protective effect of CK on islet cell apoptosis through the AMP-activated protein kinase (AMPK) mediated C-Jun N-terminal kinase (JNK) pathway. MAIN METHODS: Treatment effect of CK on type 2 diabetic (T2D) mice and palmitate-induced MIN6 ß-cells injury was observed. Fasting plasma glucose, triacylglycerol, total cholesterol, insulin levels and glucose tolerance test were evaluated. The expression of AMPK and JNK was detected in islet and MIN6 cells. KEY FINDINGS: CK treatment (30 mg/kg) decreased fasting plasma glucose, triacylglycerol, total cholesterol, elevated plasma insulin levels and improved glucose tolerance in T2D mice. CK treatment attenuated islet cell apoptosis and caspase-3 activity accompanied by a decrease in AMPK and JNK activation. Meanwhile, CK treatment attenuated the palmitate-induced reduction in MIN6 ß-cell viability, apoptosis and caspase-3 activity and activation of AMPK and JNK. The AMPK activator AICAR attenuated the CK-mediated inhibition of palmitate-induced apoptosis. SIGNIFICANCE: These data suggest that CK treatment provides a beneficial anti-diabetic effect in mice with T2D and this protective effect may be mediated through prevention of ß-cell apoptosis via inhibition of the AMPK-JNK pathway.

[Anti-proliferation action of taurine on rat cardiac fibroblast through inhibiting protein kinase Calpha expression].

This project aimed to investigate the effect of taurine on cell cycle regulatory protein p27, Cyclin D1 and nuclear factor-kappa B (NF-kappaB) p65 in the proliferation of cultured neonatal rat cardiac fibroblast (CFb) induced by angiotensin II (Ang II), and to explore the effect of taurine on the signal transduction pathway in CFb proliferation. The cultured neonatal rat CFbs were isolated by trypsin digestion method. The proliferation of CFb was induced by Ang II and detected with thiazole blue (MTT) colorimetric assay. The protein expression of p-PKCalpha in cells was determined with Western blotting technology. The expression of p27 was analyzed by flow cytometry. The expression of Cyclin D1 was determined with the combination of immunocytochemical staining and image analysis software. The nuclear translocation of NF-kappaB p65 was determined with immunofluorescence staining. Among the concentrations ranged from 40 to 160 mmol L(-1), taurine significantly inhibited p-PKCalpha expression. Taurine increased p27 expression and inhibited the nuclear translocation of NF-kappaB p65 in CFb (P < 0.05, P < 0.01, respectively) by inhibition of p-PKCalpha expression. And PKC inhibitor (Che) could improve the inhibitory action of taurine on CFb proliferation. The effects of taurine on CFb proliferation might be due to inhibition of p-PKCalpha expression and p27 expression increase and the nuclear translocation of NF-kappaB p65 inhibition followed.

[HERG K+ channel, the target of anti-arrhythmias drugs].

Rapidly activating component of delayed rectifier potassium current (I(Kr)) plays a key role in the repolarization phase of cardiac action potential. Human ether-a-go-go-related gene (HERG) encodes the alpha subunit of this potassium channel. Mutations of HERG gene induce genetic long QT syndrome (LQTS). Furthermore, I(Kr)/HERG is the target of some drugs which may cause cardiac QT interval prolongation. Some other drugs with different chemical structures also may block the channel and prolong QT interval, which even developed into acquired arrhythmias. This review summarized the recent progress of structure, gating mechanisms and functions of I(Kr)/HERG channel, I(Kr)/HERG related arrhythmias, interaction between K+ channel and drugs, and strategies of grading-up the I(Kr)/HERG target.