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H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation.
PLoS One. 2013; 8(9):e74366.Plos

Abstract

Decrease in endogenous hydrogen sulfide (H2S) was reported to participate in the pathogenesis of diabetic nephropathy (DN). This study is aimed at exploring the relationship between the abnormalities in H2S metabolism, hyperglycemia-induced oxidative stress and the activation of intrarenal renin-angiotensin system (RAS). Cultured renal mesangial cells (MCs) and streptozotocin (STZ) induced diabetic rats were used for the studies. The expressions of angiotensinogen (AGT), angiotensin converting enzyme (ACE), angiotensin II (Ang II) type I receptor (AT1), transforming growth factor-β1 (TGF-β1) and collagen IV were measured by real time PCR and Western blot. Reactive oxygen species (ROS) production was assessed by fluorescent probe assays. Cell proliferation was analyzed by 5'-bromo-2'-deoxyuridine incorporation assay. Ang II concentration was measured by an enzyme immunoassay. AGT, ACE and AT1 receptor mRNA levels and Ang II concentration were increased in high glucose (HG) -treated MCs, the cell proliferation rate and the production of TGF-β1 and of collagen IV productions were also increased. The NADPH oxidase inhibitor diphenylenechloride iodonium (DPI) was able to reverse the HG-induced RAS activation and the changes in cell proliferation and collagen synthesis. Supplementation of H2S attenuated HG-induced elevations in ROS and RAS activation. Blockade on H2S biosynthesis from cystathione-γ-lyase (CSE) by DL-propargylglycine (PPG) resulted in effects similar to that of HG treatment. In STZ-induced diabetic rats, the changes in RAS were also reversed by H2S supplementation without affecting blood glucose concentration. These data suggested that the decrease in H2S under hyperglycemic condition leads to an imbalance between oxidative and reductive species. The increased oxidative species results in intrarenal RAS activation, which, in turn, contributes to the pathogenesis of renal dysfunction.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24058553

Citation

Xue, Hong, et al. "H(2)S Inhibits Hyperglycemia-induced Intrarenal Renin-angiotensin System Activation Via Attenuation of Reactive Oxygen Species Generation." PloS One, vol. 8, no. 9, 2013, pp. e74366.
Xue H, Yuan P, Ni J, et al. H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation. PLoS ONE. 2013;8(9):e74366.
Xue, H., Yuan, P., Ni, J., Li, C., Shao, D., Liu, J., Shen, Y., Wang, Z., Zhou, L., Zhang, W., Huang, Y., Yu, C., Wang, R., & Lu, L. (2013). H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation. PloS One, 8(9), e74366. https://doi.org/10.1371/journal.pone.0074366
Xue H, et al. H(2)S Inhibits Hyperglycemia-induced Intrarenal Renin-angiotensin System Activation Via Attenuation of Reactive Oxygen Species Generation. PLoS ONE. 2013;8(9):e74366. PubMed PMID: 24058553.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation. AU - Xue,Hong, AU - Yuan,Ping, AU - Ni,Jun, AU - Li,Chen, AU - Shao,Decui, AU - Liu,Jia, AU - Shen,Yang, AU - Wang,Zhen, AU - Zhou,Li, AU - Zhang,Wei, AU - Huang,Yu, AU - Yu,Chen, AU - Wang,Rui, AU - Lu,Limin, Y1 - 2013/09/13/ PY - 2013/04/11/received PY - 2013/07/31/accepted PY - 2013/9/24/entrez PY - 2013/9/24/pubmed PY - 2014/6/17/medline SP - e74366 EP - e74366 JF - PloS one JO - PLoS ONE VL - 8 IS - 9 N2 - Decrease in endogenous hydrogen sulfide (H2S) was reported to participate in the pathogenesis of diabetic nephropathy (DN). This study is aimed at exploring the relationship between the abnormalities in H2S metabolism, hyperglycemia-induced oxidative stress and the activation of intrarenal renin-angiotensin system (RAS). Cultured renal mesangial cells (MCs) and streptozotocin (STZ) induced diabetic rats were used for the studies. The expressions of angiotensinogen (AGT), angiotensin converting enzyme (ACE), angiotensin II (Ang II) type I receptor (AT1), transforming growth factor-β1 (TGF-β1) and collagen IV were measured by real time PCR and Western blot. Reactive oxygen species (ROS) production was assessed by fluorescent probe assays. Cell proliferation was analyzed by 5'-bromo-2'-deoxyuridine incorporation assay. Ang II concentration was measured by an enzyme immunoassay. AGT, ACE and AT1 receptor mRNA levels and Ang II concentration were increased in high glucose (HG) -treated MCs, the cell proliferation rate and the production of TGF-β1 and of collagen IV productions were also increased. The NADPH oxidase inhibitor diphenylenechloride iodonium (DPI) was able to reverse the HG-induced RAS activation and the changes in cell proliferation and collagen synthesis. Supplementation of H2S attenuated HG-induced elevations in ROS and RAS activation. Blockade on H2S biosynthesis from cystathione-γ-lyase (CSE) by DL-propargylglycine (PPG) resulted in effects similar to that of HG treatment. In STZ-induced diabetic rats, the changes in RAS were also reversed by H2S supplementation without affecting blood glucose concentration. These data suggested that the decrease in H2S under hyperglycemic condition leads to an imbalance between oxidative and reductive species. The increased oxidative species results in intrarenal RAS activation, which, in turn, contributes to the pathogenesis of renal dysfunction. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/24058553/H_2_S_inhibits_hyperglycemia_induced_intrarenal_renin_angiotensin_system_activation_via_attenuation_of_reactive_oxygen_species_generation_ L2 - http://dx.plos.org/10.1371/journal.pone.0074366 DB - PRIME DP - Unbound Medicine ER -