Adiponectin acts as an endogenous antithrombotic factor. However, the mechanisms underlying the inhibition of platelet aggregation by adiponectin still remain elusive. The present study was designed to test whether adiponectin inhibits platelet aggregation by attenuation of oxidative/nitrative stress. Adult rats were fed a regular or high-fat diet for 14 weeks. The platelet was immediately separated and stimulated with recombinant full-length adiponectin (rAPN) or not. The platelet aggregation, nitric oxide (NO) and superoxide production, endothelial nitric oxide synthase (eNOS)/inducible NOS (iNOS) expression, and antioxidant capacity were determined. Treatment with rAPN inhibited hyperlipidemia- induced platelet aggregation (P<0.05). Interestingly, total NO, a crucial molecule depressing platelet aggregation and thrombus formation , was significantly reduced, rather than increased in rAPN-treated platelets. Treatment with rAPN markedly decreased superoxide production (-62 %, P<0.05) and enhanced antioxidant capacity (+38 %, P<0.05) in hyperlipidemic platelets. Hyperlipidemia-induced reduced eNOS phosphorylation and increased iNOS expression were significantly reversed following rAPN treatment (P<0.05, P<0.01, respectively). Taken together, these data suggest that adiponectin is an adipokine that suppresses platelet aggregation by enhancing eNOS activation and attenuating oxidative/nitrative stress including blocking iNOS expression and superoxide production., W.-Q. Wang ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The effects of chilling treatment (4 °C) under low irradiance, LI (100 μmol m-2 s-1) and in the dark on subsequent recovery of photosynthesis in chilling-sensitive sweet pepper leaves were investigated by comparing the ratio of quantum yields of photosystem (PS) 2 and CO2 assimilation, ΦPS2/ΦCO2, measured in normal air (21 % O2, NA) and low O2-air (2% O2, LOA), and by analyzing chlorophyll (Chl) a fluorescence parameters. Chilling treatment in the dark had little effect on Fv/Fm and ΦPS2/ΦCO2, but it caused the decrease of net photosynthetic rate (PN) under saturating irradiance after 6-h chilling treatment, indicating that short-term chilling alone did not induce PS2 photoinhibition. Furthermore, photorespiration and Mehler reaction also did not obviously change during subsequent recovery after chilling stress in the dark. During chilling treatment under LI, there were obvious changes in Fv/Fm and ΦPS2/ΦCO2, determined in NA or LOA. Fv/Fm could recover fully in 4 h at 25 °C, and ΦPS2/ΦCO2 increased at the end of the treatment, as determined in both NA and LOA. During subsequent recovery, ΦPS2/ΦCO2 in LOA decreased faster than in NA. Thus the Mehler reaction might play an important role during chilling treatment under LI, and photorespiration was an important process during the subsequent recovery. The recovery of PN under saturating irradiance determined in NA and LOA took about 50 h, implying that there were some factors besides CO2 assimilation limiting the recovery of photosynthesis. From the progress of reduced P700 and the increase of the Mehler reaction during chilling under LI we propose that active oxygen species were the factors inducing PS1 photoinhibition, which prevented the recovery of photosynthesis in optimal conditions because of the slow recovery of the oxidizable P700. and X.-G. Li ... [et al.].