Oxidative stress plays an important role in pressure overloadinduced
cardiac remodeling. The purpose of this study was to determine whether apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, attenuates pressure overload-induced cardiac remodeling in rats. After abdominal aorta constriction, the surviving rats were randomly divided into four groups: sham group, abdominal aorta constriction group, apocynin group, captopril group. Left ventricular pathological changes were studied using Masson’s trichrome staining. Metalloproteinase-2 (MMP-2) levels in the left ventricle were analyzed by western blot and gelatin zymography. Oxidative stress and apoptotic index were also examined in cardiomyocytes using dihydroethidium and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), respectively. Our results showed that abdominal aorta constriction significantly caused excess collagen deposition and cardiac insult. Treatment with apocynin significantly inhibited deposition of collagen and reduced the level of MMP-2. Furthermore, apocynin also decreased the NADPH oxidase activity, reactive oxygen species production and cardiomyocyte apoptotic index. Interestingly, apocynin only inhibited NADPH oxidase activity without affecting its expression or the level of angiotension II in the left ventricle. In conclusion, apocynin reduced collagen deposition, oxidative stress, and inhibited apoptosis, ultimately ameliorating cardiac remodeling by mechanisms that are independent of the renin-angiotensin system.
Calligonum caput-medusae is known to grow well when irrigated with water containing NaCl. The aim of this study was to investigate ecophysiological responses of C. caput-medusae to different NaCl concentrations. In our study, we examined the effect of 0, 50, 100, 200, and 400 mM NaCl. Our results demonstrated that maximum seedling growth occurred at 50 mM NaCl. Photosynthetic parameters, such as the photosynthetic pigment content and gas exchange parameters, correlated with growth response. High salinity (≥ 100 mM NaCl) resulted in a significant reduction of the plant growth. Similarly, marked declines in the pigment content, maximal efficiency of PSII photochemistry, net photosynthetic rate, transpiration rate, and stomatal conductance were also detected. However, intercellular CO2 concentration showed a biphasic response, decreasing with water containing less than 200 mM NaCl and increasing with NaCl concentration up to 400 mM. Water-use efficiency and intrinsic water-use efficiency exhibited the opposite response. The reduction of photosynthesis at the high NaCl concentration could be caused by nonstomatal factors. High salinity led also to a decrease in the relative water content and water potential. Correspondingly, an accumulation of soluble sugars and proline was also observed. Na+ and
Cl- concentrations increased in all tissues and K+ concentrations were maintained high during exposure to NaCl compared with the control. High salinity caused oxidative stress, which was evidenced by high malondialdehyde and hydrogen peroxide contents. In order to cope with oxidative stress, the activity of antioxidative enzymes increased to maximum after 50 mM NaCl treatment. The data reported in this study indicate that C. caput-medusae can be utilized in mild salinity-prone environments., Y. Lu, J.-Q. Lei, F.-J. Zeng, B. Zhang, G.-J. Liu, B. Liu, X.-Y. Li., and Obsahuje bibliografii
Salusin-β is newly identified bioactive peptide of 20 amino acids, which is widely distributed in hematopoietic system, endocrine system, and the central nervous system (CNS). Although salusin- β extensively expressed in the CNS, the central cardiovascular functions of salusin-β are unclear. Our main objective was to determine the cardiovascular effect of microinjection of salusin-β into the nucleus tractus solitarii (NTS) in anesthetized rats. Bilateral or unilateral microinjection of salusin-β (0.94-94 μg/rat) into the NTS dose-dependently decreased blood pressure and heart rate. Bilateral NTS microinjection of salusin-β (9.4 μg/rat) did not alter baroreflex sensitivity. Prior application of the glutamate receptor antagonist kynurenic acid (0.19 μg/rat, n=9) into the NTS did not alter the salusin-β (9.4 μg/rat) induced hypotension and bradycardia. However, pretreatment with the GABA receptor agonist muscimol (0.5 ng/rat) within the rostral ventrolateral medulla (RVLM) completely abolished the hypotension (-14±5 vs. -3±5 mm Hg, P <0.05) and bradycardia (-22±6 vs. -6±5 bpm, P <0.05) evoked by intra-NTS salusin-β (9.4 μg/rat). In addition, we found that vagotomy didn’t influence the actions of salusin-β (9.4 μg/rat) in the NTS. In conclusion, our present study shows that microinjection of salusin-β into the NTS significantly produces hypotension and bradycardia, presumably by suppressing the activities of presympathetic neurons in the RVLM., Y. Lu, Y. S. Wu, D. S. Chen, M. M. Wang, W. Z. Wang, W. J. Yuan., and Obsahuje bibliografii
RNA editing is post-transcriptional modification to RNA molecules. In plants, RNA editing primarily occurs to two energy-producing organelles: plastids and mitochondria. Organelle RNA editing is often viewed as a mechanism of correction to compensate for defects or mutations in haploid organelle genomes. A common type of organelle RNA editing is deamination from cytidine to uridine. Cytidine-to-uridine plastid RNA editing is carried out by the RNA editing complex which consists of at least four types of proteins: pentatricopeptide repeat proteins, RNA editing interacting proteins/multiple organellar RNA editing factors, organelle RNA recognition motif proteins, and organelle zinc-finger proteins. The four types of RNA editing factors work together to carry out RNA editing site recognition, zinc cofactor binding, and cytidine-to-uridine deamination. In addition, three other types of proteins have been found to be important for plastid RNA editing. These additional proteins may play a regulatory or stabilizing role in the RNA editing complex., Y. Lu., and Obsahuje bibliografické odkazy
Hydrogen sulfide (H2S), an endogenous “gasotransmitter”, exists in the central nervous system. However, the central cardiovascular effects of endogenous H2S are not fully determined. The present study was designed to investigate the central cardiovascular effects and its possible mechanism in anesthetized rats. Intracerebrovent ricular (icv) injection of NaHS (0.17~17 μ g) produced a significant and dose-dependent decrease in blood pressure (BP) and heart rate (HR) (P<0.05) compared to control. The higher dose of NaHS (17 μ g, n=6) decreased BP and HR quickly of rats and 2 of them died of respiratory paralyse. Icv injection of the cystathionine beta-synthetase (CBS) activator s-adenosyl-L-methionine (SAM, 26 μ g) also produced a significant hypotension and bradycardia, which were similar to the results of icv injection of NaHS. Furthermore, the hypotension and bradycardia induced by icv NaHS were effectively attenuated by pretreatment with the KATP channel blocker glibenclamide but not with the CBS inhibitor hydroxylamine. The present study suggests that icv injection of NaHS produces hypotension and bradycardia, which is dependent on the KATP channel activation., W.-Q. Liu ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy