[Effects of ultrasound on the germination and seedling growth of three aged forage seeds.] / è¶ å£°æ³¢å¯¹3种老化牧草种子萌发和幼苗生长的影响.

To examine the effects and physiological mechanisms of ultrasound treatment on the germination and seedling growth of naturally aged seeds, an [L9(34)] orthogonal matrix experiment was carried out, which included ultrasound time, ultrasound temperature, output power and seed soaking time with tall fescue Festuca arundinacea stored for one year and five years at room temperature, perennial ryegrass (Lolium perenne, stored for five years), and Russian wildrye (Psathyrostachys juncea, stored for six years) as test materials. The results showed that ultrasound temperature was the most important factor for the germination of aged seeds. The appropriate ultrasound treatment promoted germination percentage and significantly enhanced root and shoot length in aged seeds of tall fescue (stored for five years) and Russian wildrye. The positive effect of ultrasound was not significant on the germination of aged seeds of tall fescue (stored for one year) and perennial ryegrass, but was significant on the root length. Ultrasound treatment reinvigorated aged seeds by increasing superoxide dismutase (SOD) and peroxidase (POD) activities and reducing malondialdehyde (MDA) content. A regression model analysis was performed to determine the final optimal ultrasound condition for aged grass seeds that resulted in ultrasound time of 22 min, at 26 ℃, output power of 254.29 W and a seed soaking time of 2.89 h.

Astaxanthin attenuated pressure overload-induced cardiac dysfunction and myocardial fibrosis: Partially by activating SIRT1.

BACKGROUND: Myocardial fibrosis contributes to cardiac dysfunction. Astaxanthin (AST), a member of the carotenoid family, is a well-known antioxidant, but its effect on and underlying mechanisms in myocardial fibrosis are poorly understood. METHODS: In vivo, myocardial fibrosis and cardiac dysfunction were induced using transverse aortic constriction (TAC). AST was administered to mice for 12weeks post-surgery. In vitro, transforming growth factor ß1 (TGF-ß1) was used to stimulate human cardiac fibroblasts (HCFs). EX-527 (6-chloro-2, 3, 4, 9-tetrahydro-1H-carbazole-1-carboxamide) and SIRT1 siRNA were used to inhibit SIRT1 in vivo and in vitro, respectively. The effects of AST on cardiac function and fibrosis were determined. SIRT1 expression and activity were measured to explore the mechanisms underlying its effects. RESULTS: AST improved cardiac function and attenuated fibrosis. Receptor activated-SMADs (R-SMADs), including SMAD2 and SMAD3, played important roles in these processes. The TAC surgery-induced increases in the expression of phosphorylated and acetylated R-SMADs were attenuated by treatment with AST, the translocation and transcriptional activity of R-SMADs were also restrained. These effects were accompanied by an increase in the expression and activity of SIRT1. Inhibiting SIRT1 attenuated the acetylation and transcriptional activity of R-SMADs, but not their phosphorylation and translocation. CONCLUSIONS: Our data demonstrate that AST improves cardiac function and attenuates fibrosis by decreasing phosphorylation and deacetylation of R-SMADs. SIRT1 contributes to AST's protective function by reducing acetylation of R-SMADs. GENERAL SIGNIFICANCE: These data suggest that AST may be useful as a preventive/therapeutic agent for cardiac dysfunction and myocardial fibrosis.

Restoration of Mimecan Expression by Grape Seed Procyanidin B2 Through Regulation of Nuclear Factor-kappaB in Mice With Diabetic Nephropathy.

Grape seed procyanidin B2 (GSPB2) exerts a variety of potent protective pharmacological effects on diabetic complications. The renal protective effects of GSPB2 and the target protein mimecan regulated by GSPB2, discovered in a previous quantitative proteomic analysis, were assessed in mice with diabetic nephropathy Twenty-four db/db mice were divided into 2 groups of the vehicle-treated and GSPB2-treated (30 mg/kg/d) diabetic groups. All animals were observed for 10 weeks. Treatment with GSPB2 resulted in an improvement in body weight increase and serum levels of triglyceride, total cholesterol, advanced glycation end products, and urinary albumin excretion in comparison with the vehicle-treated diabetic mice (P < .05), although these levels were still higher than those in the control group. Treatment with GSPB2 significantly reduced the extent of glomerular basement membranes thickening, mesangial expansion, and glomerular area as well. Mimecan protein expressions in diabetes mellitus were decreased approximately by 28% when compared with those in the control group (P < .05), and restored remarkably after GSPB2 treatment (P < .05). The expression of nuclear factor-κB (NF-κB) p65 in nuclear extracts, markedly higher in the diabetic mice than in the controls, was significantly suppressed by GSPB2. The findings of this study revealed that mimecan might become a new therapeutic target in the future and indicated that GSPB2 had beneficial effects not only on oxidative stress, but also on renal fibrosis, particularly in the diabetic kidney.

[Advances in research on mechanisms of seed pre-treatments.] / ç§å­é¢„å¤„ç†çš„ä½œç”¨æœºåˆ¶ç ”ç©¶è¿›å±•.

Seeds play a vital role in nature and agro-ecosystems. The success of seed germination and the establishment of a normal seedling determine the propagation and survival of a plant species, but seed vigor is often seriously damaged because of seed aging, dormancy and the deterioration of natural habitat. Thus, exploring methods for improving germination quality is of great significance to ecology and the economy. Based on the latest international reports, seed pre-treatments are the most practical and effective methods for improving plant performance, increasing yields and enhancing stress resistance. This review provided a summary of the current pre-sowing treatment technologies and the physiological and biochemical responses of plants to these methods by addressing gene expression, cytological effects, enzyme system activities, material and energy metabolism, antioxidation mechanisms and signal transduction pathways. We also interpreted the mechanisms of the seed pre-treatment methods from aspects of seed germination acceleration and stress resistance enhancement. The bottleneck in seed pre-treatments at the cytological and molecular levels and the problems involved in their application were also discussed. Thus far, most studies had largely focused on the partial reaction alterations of plant biochemistry and enzyme activities, and they had generally been characterized by a lack of systematic and holistic study for applications to crop production. Finally, we proposed an outlook for further study in an attempt to provide a prospective and scientific reference for plant germplasm conservation, high-efficiency organic agriculture development and ecological environment re-construction.

Cofilin1 is involved in hypertension-induced renal damage via the regulation of NF-κB in renal tubular epithelial cells.

BACKGROUND: Inflammation mediated by nuclear factor-κB (NF-κB) plays a critical role in the pathogenesis of hypertensive nephropathy (HN). Cytoskeletal remodelling is necessary for the activation of NF-κB. An actin-binding protein, cofilin-1 promotes dynamic alterations to the cytoskeleton by severing actin filaments. However, whether cofilin1 modulates NF-κB activity via cytoskeletal remodelling in the setting of hypertensive renal damage and what mechanisms underlie this phenomenon, remain unknown. METHODS: Twenty-one-week old spontaneously hypertensive rats (SHRs) were treated with an antioxidant (100 or 250 mg kg(-1) day(-1)), grape seed proanthocyanidins extract (GSPE), for 22 weeks. Twenty-four-hour urinary protein, serum creatinine and urea nitrogen levels were measured. Haematoxylin and eosin (HE) staining was performed, and the expression levels of renal cortex cofilin1, monocyte chemotactic protein 1 (MCP1), interleukin-1ß (IL1ß) and NF-κB were evaluated via either Western blotting or immunohistochemistry. In vitro, human proximal renal tubular epithelial cells (HK-2 cells) were pre-incubated either with or without GSPE and subsequently treated with angiotensinII (AngII). Furthermore, a lentiviral shRNA-vector was utilized to knockdown cofilin1 expression in the HK-2 cells, which were stimulated with AngII. Actin filaments, NF-κB activity and several downstream inflammatory factors, including MCP1 and IL-1ß, were investigated. RESULTS: In addition to elevated blood pressure and 24 h urinary protein levels, NF-κB activity and the expression levels of MCP1 and IL-1ß were significantly increased, resulting in tubulointerstitial inflammatory infiltration in SHRs. The phosphorylation (inactivation) of cofilin1 was increased in the kidneys of the SHRs. In vitro, AngII stimulation resulted in the phosphorylation of cofilin1, the formation of actin stress fibres and nuclear translocation of NF-κB p65 in the HK2 cells. Both GSPE pretreatment and the shRNA knockdown of cofilin1 inhibited Rel/p65 nuclear translocation, as well as the expression of both MCP-1 and IL-1ß in the AngII-induced HK2 cells. CONCLUSION: These results demonstrate that cofilin1 is involved in hypertensive nephropathy by modulating the nuclear translocation of NF-κB and the expression of its downstream inflammatory factors in renal tubular epithelial cells.