title: [Exogenous hydrogen sulfide reduces vascular aging in D-galactose-induced subacute aging rats].
abstract: The present study was aimed to observe the protective effect of exogenous hydrogen sulfide (H₂S) on vascular structural and functional changes of aorta in D-galactose-induced subacute aging rats. Adult male SD rats were randomly divided to five groups: the vehicle group, the D-galactose (D-gal) group, and the three NaHS groups treated with low (1 μmol·kg⁻¹·d⁻¹), middle (10 μmol·kg⁻¹·d⁻¹) or high (100 μmol·kg⁻¹·d⁻¹) dose of NaHS respectively. The D-gal group rats were given subcutaneously injection of 125 mg/kg D-gal per day for eight weeks to induce subacute aging model. In the NaHS group, D-gal was administered as above but with NaHS intraperitoneally injected at a dosage of 1, 10, 100 μmol·kg⁻¹·d⁻¹ respectively. Equivalent volumes of saline were administered per day for eight weeks in vehicle group. Morphological changes of aorta were observed by HE and Masson staining. The level of H₂S in serum, the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA), as well as anti-superoxide anions in vascular tissue were determined by spectrophotometry. Angiotensin II (AngII) levels in plasma were measured using competitive enzyme immunoassay. The expression of angiotensin II type 1 receptor (AT1R) in aorta was determined by Western blot. The results showed that the aging aortic morphologic changes in model rats were ameliorated in NaHS groups. Decreased vascular endothelial exfoliative cells and vascular smooth muscle cell (SMC) proliferation were shown in NaHS groups by HE staining. Masson staining analysis showed reduced relative contents of collagen fibers (P < 0.05) and SMC (P < 0.05) in NaHS groups. Compared to vehicle group, serum concentration of H₂S in D-gal group was decreased, while it was increased in NaHS groups after treatment with NaHS (P < 0.05). In the D-gal group, the concentration of AngII in plasma was significantly increased compared with that in vehicle group, while it was decreased in NaHS groups (P < 0.05). Moreover, levels of vascular tissue anti-superoxide anion and the activity of SOD were obviously higher, MDA was significantly lower in all NaHS treated groups than those in the D-gal group respectively (P < 0.05). Western blot analysis showed that the expression of AT1R was increased in D-gal group compared with that in vehicle group, while it was decreased after treatment with NaHS compared with that in D-gal group (P < 0.05). These results suggest that exogenous H₂S can ameliorate the age-related changes of aortic morphology, decrease the concentration of AngII in plasma, down-regulate the expression of AT1R in vascular tissue, and mitigate the level of oxidative stress. These changes delay the vascular aging in aging rats ultimately.
authors: Department of Physiology; Institute of Cardiovascular Disease; Department of Pathology; Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China. yancd55@163.com.
authors: Wei-Li
authors: WL
authors: Qiao
authors: Wen-Xue
authors: WX
authors: Yang
authors: Lei
authors: L
authors: Liu
authors: Yue
authors: Y
authors: Shi
authors: Jie
authors: J
authors: Cui
authors: Hong
authors: H
authors: Liu
authors: Chang-Dong
authors: CD
authors: Yan
mesh_terms: D000375:Aging / Q000187:drug effects*; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000473:pathology*; D049109:Cell Proliferation; D042783:Endothelial Cells / Q000378:metabolism; D005690:Galactose / Q000009:adverse effects; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D044139:Receptor, Angiotensin, Type 2; D013440:Sulfides; D000804:Angiotensin II; D008315:Malondialdehyde; D013482:Superoxide Dismutase; C025451:sodium bisulfide; D005690:Galactose; D006862:Hydrogen Sulfide