Objective-We explored the effect of hydrogen sulfide (H 2 S) on atherosclerotic progression, particularly on intracellular adhesion molecule-1 (ICAM-1) in apolipoprotein-E knockout (apoE Ϫ/Ϫ ) mice and human umbilical vein endothelial cells (HUVECs). Methods and Results-ApoEϪ/Ϫ mice were treated with sodium hydrosulfide (NaHS) or DL-propargylglycine (PPG); HUVECs were pretreated with NaHS. Compared with control mice, apoE Ϫ/Ϫ mice showed decreased plasma H 2 S level and aortic H 2 S production but increased plasma ICAM-1 and aortic ICAM-1 protein and mRNA. Compared with apoE Ϫ/Ϫ mice, apoE Ϫ/Ϫ ϩNaHS mice showed increased plasma H 2 S level, but decreased size of atherosclerotic plaque and plasma and aortic ICAM-1 levels, whereas apoE Ϫ/Ϫ ϩPPG mice showed decreased plasma H 2 S level but enlarged plaque size and increased plasma and aortic ICAM-1 levels. NaHS suppressed ICAM-1 expression in tumor necrosis factor (TNF)-␣-treated HUVECs. NaHS inhibited IB degradation and NF-B nuclear translocation in HUVECs treated with TNF-␣. Ⅲapolipoprotein E knockout mice Ⅲ human umbilical vein endothelial cells A therosclerosis is an important underlying pathology of cardiovascular diseases, the leading cause of morbidity and mortality in many countries. Over the past 50 years, numerous studies attempting to explain the complex events leading to atherosclerosis have been undertaken. Nitric oxide and carbon monoxide, which are small gaseous transmitters, freely permeable to membrane, endogenously and enzymatically generated, and have specific functions, are recommended as gasotransmitters. 1 They have been closely implicated in endothelial dysfunction and vascular remodeling in atherosclerotic arteries; researches into the two gasotransmitters have improved the understanding of atherogenesis. [2][3][4][5] However, the mechanisms of atherosclerosis have not been fully elucidated. Conclusions-The

The mechanisms responsible for the cardioprotective effect of hydrogen sulfide (H(2)S) are unclear. The present study was designed to examine whether H(2)S could regulate hyperhomocysteinemia (HHcy)-induced cardiomyocytic endoplasmic reticulum (ER) stress. A rat model of HHcy was produced, and H9c2 cells (rat embryonic heart-derived cell line) were cultured. The plasma homocysteine was measured by using HPLC. Plasma H(2)S concentration and myocardial H(2)S production were measured with a sulfide-sensitive electrode. Confocal immunofluorescent analysis for cardiomyocytic C/EBP homologous protein (CHOP) was performed. Glucose-regulated protein 78 (GRP78), CHOP, and caspase 12 expressions by myocardial tissues and cleaved caspase 12 and p-eIF2alpha expressions by H9c2 cells were detected with Western blotting. The results showed that methionine overload induced HHcy, resulting in a marked cardiomyocytic ER stress, whereas endogenous production of H(2)S was reduced in rats with HHcy. H(2)S supplementation, however, decreased expressions of ER stress-associated proteins, including GRP78, CHOP, and caspase 12, by myocardial tissues in vivo. The inhibition of endogenous H(2)S production further enhanced cardiomyocytic ER stress, but H(2)S supplementation effectively antagonized the H9c2 cell CHOP, cleaved caspase 12 and p-eIF2alpha expressions induced by Hcy, thapsigargin, or tunicamycin in vitro. The results suggest that H(2)S can attenuate cardiomyocytic ER stress in HHcy-induced cardiomyocytic injury.

Aim: To investigate the modulatory effect of sudium hydrosulfide on lung tissue‐oxidized glutathione and total antioxidant capacity in the development of hypoxic pulmonary hypertension (HPH). Methods: After 21 d of hypoxia, the mean pulmonary artery pressure was measured by cardiac catheterization. The plasma H2S level and production of H2S in the lung tissues were determined by using a spectrophotometer. The lung homogenates were assayed for total antioxidant capacity (T‐AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione and malonaldehyde by colorimetry. The mRNA level of SOD was analyzed by real‐time PCR, and the SOD expression was detected by Western blotting. Results: In the hypoxia group, the plasma H2S concentration and H2S production in the lung was significantly decreased compared with the control group (187.2±13.1 vs 299.6±12.4 μmol/L; 0.138±0.013 vs 0.289±0.036 nmol·mg−1·min−1, P<0.01). The administration of sodium hydrosulfide could reduce the mean pulmonary artery pressure by 31.2% compared with the hypoxia group (P<0.01). Treatment with sodium hydrosulfide decreased GSSG, and the T‐AOC level of the lung tissues was enhanced compared with the hypoxia group (P<0.05). There were no significant changes in the lung tissue SOD mRNA level, protein level, and its activity among the 3 groups. Conclusion: Oxidative stress occurred in the development of HPH and was accompanied by a decrease in the endogenous production of H2S in the lung tissues. H2S acted as an antioxidant during the oxidative stress of HPH partly as a result of the attenuated GSSG content.

Aim: The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO 2 ) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. Methods: Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-β-hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO 2 group receiving MCT plus SO 2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO 2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. Results: In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO 2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDX-treated rats, lung tissues and plasma SO 2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCTtreated rats (P<0.01). In contrast, with the use of a SO 2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels. Conclusion: Endogenous SO 2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.

BackgroundScylla paramamosain (Crustacea: Decapoda: Portunidae: Syclla De Hann) is a commercially important mud crab distributed along the coast of southern China and other Indo-Pacific countries (Lin Z, Hao M, Zhu D, et al, Comp Biochem Physiol B Biochem Mol Biol 208-209:29–37, 2017; Walton ME, Vay LL, Lebata JH, et al, Estuar Coast Shelf Sci 66(3–4):493–500, 2006; Wang Z, Sun B, Zhu F, Fish Shellfish Immunol 67:612–9, 2017). While S. paramamosain is a euryhaline species, a sudden drop in salinity induces a negative impact on growth, molting, and reproduction, and may even cause death. The mechanism of osmotic regulation of marine crustaceans has been recently under investigation. However, the mechanism of adapting to a sudden drop in salinity has not been reported.MethodsIn this study, transcriptomics analysis was conducted on the gills of S. paramamosain to test its adaptive capabilities over 120 h with a sudden drop in salinity from 23 ‰ to 3 ‰.ResultsAt the level of transcription, 135 DEGs (108 up-regulated and 27 down-regulated) annotated by NCBI non-redundant (nr) protein database were screened. GO analysis showed that the catalytic activity category showed the most participating genes in the 24 s-tier GO terms, indicating that intracellular metabolic activities in S. paramamosain were enhanced. Of the 164 mapped KEGG pathways, seven of the top 20 pathways were closely related to regulation of the Na+ / K+ -ATPase. Seven additional amino acid metabolism-related pathways were also found, along with other important signaling pathways.ConclusionIon transport and amino acid metabolism were key factors in regulating the salinity adaptation of S. paramamosain in addition to several important signaling pathways.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4803-x) contains supplementary material, which is available to authorized users.