Effects of 3,4-dihydroxyacetophenone on the hypercholesterolemia-induced atherosclerotic rabbits.

3,4-Dihydroxyacetophenone (3,4-DHAP) is one herbal extract from bald Mao-dong-qing leaves. We reported that 3,4-DHAP had anti-inflammatory function by decreasing tumor necrosis factor-α (TNF-α) secretion in macrophages. The aim of the study was to examine the effects of 3,4-DHAP on plasma and liver lipids, plasma alanine aminotranferase (ALT) and TNF-α level, vascular cell adhesion molecule-1 (VCAM-1) expression, plaque vulnerability and vascular inflammation in hypercholesterolemia-induced atherosclerotic rabbits. Male New Zealand white rabbits were randomized into negative control, positive control, 3,4-DHAP and simvastatin groups. From weeks 2 to 12, the rabbits were treated with 3,4-DHAP or simvastatin. At weeks 12, all the animals were sacrificed. Plasma lipids and ALT were measured using the enzymatic endpoint method. Plasma TNF-α was measured using enzyme-linked immuno sorbent assay (ELISA). Liver lipids concentrations were estimated using commercial kits. The expression of VCAM-1 was measured using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Histological analysis was used to evaluate the pathologic changes of rabbit aortas. The results showed that 3,4-DHAP markedly lowered plasma and liver lipids, lowered plasma ALT and TNF-α levels compared with the positive control group. VCAM-1 mRNA and protein were markedly inhibited by 3,4-DHAP. Decreased aortic plaque instability was evident in 3,4-DHAP-treated rabbits, as demonstrated by a thickened elastic layer, increased vascular smooth muscle cells (VSMCs) accumulation in the plaques, less neointima hyperplasia and macrophages recruitment. 3,4-DHAP may attenuate the progression of atherosclerotic lesions and stabilize plaques by lowering plasma lipids, the number of macrophages and the expression of VCAM-1, while increasing the number of VSMCs in the atherosclerotic plaques.

Proteomics analysis reveals the defense priming effect of chitosan oligosaccharides in Arabidopsis-Pst DC3000 interaction.

Chitosan oligosaccharides (COS) worked effectively in multiple plant-pathogen interactions as plant immunity regulator, however, due to the complexity of the COS-induced immune signaling network, the topic requires further investigation. In the present study, quantitative analysis of proteins was performed to investigate the underlying mechanism of COS induced resistance to Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) in Arabidopsis thaliana. 4303 proteins were successfully quantified, 186, 217 and 207 proteins were differently regulated in mock + Pst, COS, and COS + Pst treated plants, respectively, compared with mock plants. From detailed functional and hierarchical clustering analysis, a priming effect of COS on plant immune system by pre-regulated the key proteins related to signaling transduction, defense response, cell wall biosynthesis and modification, plant growth and development, gene transcription and translation, which confers enhanced resistance when Pst DC3000 infection in Arabidopsis. Moreover, RACK1B which has the potential to be the key kinase receptor for COS signals was found out by protein-protein interaction network analysis of COS responsive proteins. In conclusion, COS treatment enable plant to fine-tuning its defense mechanisms for a more rapid and stronger response to future pathogen attacks, which obviously enhances plants defensive capacity that makes COS worked effectively in multiple plant-pathogen interactions.

Alginate Oligosaccharide (AOS) induced resistance to Pst DC3000 via salicylic acid-mediated signaling pathway in Arabidopsis thaliana.

Alginate Oligosaccharide (AOS) is a natural biological carbohydrate extracted from seaweed. In our study, Arabidopsis thaliana was used to evaluate the AOS-induced resistance to Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). Resistance was vitally enhanced at 25 mg/L in wild type (WT), showing the decreased disease index and bacteria colonies, burst of ROS and NO, high transcription expression of resistance genes PR1 and increased content of salicylic acid (SA). In SA deficient mutant (sid2), AOS-induced disease resistance dropped obviously compared to WT. The disease index was significantly higher than WT and the expression of recA and avrPtoB are two and four times lower than WT, implying that AOS induces disease resistance injecting Pst DC3000 after three days treatment by arousing the SA pathway. Our results provide a reference for the profound research and application of AOS in agriculture.

Protective role of α-lipoic acid in hyperuricemia-induced endothelial dysfunction.

The aim of the current study was to determine the effects of α-lipoic acid (LA) on hyperuricemia and endothelial dysfunction, and to uncover the underlying mechanism of its action. A hyperuricemic rat model was established by administration of uric acid (UA) and the rats were orally fed with 2 g/kg/day LA or phosphate-buffered saline. Primary rat aortic endothelial cells were subsequently isolated, and a cell viability assay, apoptosis assay, enzyme nitric oxide synthase (eNOS) activity assay and mitochondrial function assay were all performed. For the in vitro study, human umbilical vein endothelial cells were used and western blotting was performed to assess Akt signaling activity. The results of the current study indicated that LA inhibited apoptosis, enhanced eNOS activity and production of nitric oxide (NO), and rescued mitochondrial mass and function in uric acid (UA)-treated endothelial cells. LA activated Akt signaling and inhibition of Akt signaling abolished the effects of LA on cell viability, NO production, ROS production and ATP levels in UA-treated endothelial cells. Therefore, the current study demonstrated that LA attenuated oxidant stress and inhibited apoptosis in UA-treated endothelial cells by activating Akt signaling. The results indicate that LA may serve as a therapeutic approach to treat hyperuricemia-induced endothelial dysfunction.