title: [Effect of hydrogen sulfide on antiatherosclerosis in rats].
abstract: OBJECTIVE
  To investigate the effect of hydrogen sulfide (H2S) on artherosclerosis (AS) and its mechanism in rats.
  
  
  METHODS
  125 healthy male SD rats of the weight (210 +/- 10) g were randomly divided into 5 groups: control group, AS model group, AS + low-dose NaHS (2.8 micromol/(kg x d)) group, AS+ middle-dose (14 micromol/(kg x d)) NaHS group, AS+ high-dose NaHS (28 micromol/(kg x d)) group. The atherosclerotic model was established by feeding high grease food and injecting large doses of VitD3. The rats were using NaHS by peritoneal injection for 12 weeks. 5 rats were executed in each group before the experiment and in the weeks of 3, 6, 9, 12 after the experiment, respeotively. The blood fat was analyzed by automatic biochemistry analysator. H2S content in serum was detected by the method of deproteinization. The pathological damage of vessels was observed and scored by HE stain. The expression of VEGF in the vessel tissue was detected by immunohistochemistry staining.
  
  
  RESULTS
  Compared with the control group at contemporaneity, both serumal triglyceride (TG) and cholesterol (TC) increased significantly in the AS model group after rat feeded 3, 6, 9, 12 weeks, and scores of the artery pathological damage also increased obviously from the 6th week to the 12th week (P < 0.01), as well as artherosclerosis plaque appeared, displaying as lipid plaque in the positive part. The serumal H2S concentration decreased obviously, from (44.98 +/- 2.06) micromol/L of before feeding to (38.56 +/- 2.26), (32.96 +/- 2.38), (28.63 +/- 0.92), (23.55 +/- 0.92) nnol/L of after feeding 3, 6, 9, and 12 weeks, respectively, and lower than that of control at contemporaneity (44.72 +/- 0.85), (43.71 +/- 0.59), (41.96 +/- 0.97), (39.87 +/- 1.25) micromol/L, respectively ( P < 0.01), and VEGF expression of the vascular tissue also increased (P < 0.01). Compared with the AS model group, all of above indexes in rat of the low-dose of NaHS group did not appear any obvious change. The serumal H2S concentration in rat of the middle-dose NaHS began increase at the 6 week after rat feeded (36.13 +/- 0.3 vs. 32.96 +/- 2.38 micronol/L, P < 0.05), and continuously increased at the 9th and the 12th week (33.07 +/- 1.14 vs. 28.63 +/- 0.92 micromol/L, 30.16 +/- 0.2 vs. 23.55 +/- 0.92 micromol/L; P < 0.01, respectively). The serumal H2S concentration in high-dose NaHS groups, increased from the 3th to the 12th week (41.25 +/- 0.80, 38.71 +/- 0.46, 35.31 +/- 0.62, 33.38 +/- 0.78 micromol/L, respectively, P < 0.01). The rat serumal TC in both middle and high-dose NaHS groups, decreased from the 3th to the 12th week (P < 0.01), and TG began decrease from the 3th and the 6th week to the 12th week after rat feeded, respectively (P < 0.05, P < 0.01). Both of the pathological damage scores and the expression of VEGF decrease from the 6th week to the 12th week (P < 0.05). The correlation analysis showed that H2S in serum had a negative correlation with both pathological damage scores (r = -0.917, P < 0.01) and the expression of VEGF (r = -0. 885, P < 0.01). But it had no obvious correlation with serumal TG and TC.
  
  
  CONCLUSIONS
  The formation and development of artherosclerosis has a close correlation with the depressing of endogenous H2S. Administration of exogenous H2S could raise the H2S concentration of serum in artherosclerosis, which might improve the damage of vessels and inhibit the expression of VEGF.
authors.affiliation: Department of Physiology, School of Basic Medicine, Wuhan University, China.
authors.forename: Shi-jian
authors.initials: SJ
authors.lastname: Chen
authors.forename: Xiao-hongl
authors.initials: XH
authors.lastname: Yan
authors.forename: Xiao-yingt
authors.initials: XY
authors.lastname: Zhu
authors.forename: Min
authors.initials: M
authors.lastname: Hu
authors.forename: Sheng-guo
authors.initials: SG
authors.lastname: Hu
authors.forename: Wen-jun
authors.initials: WJ
authors.lastname: Yuan
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000503:physiopathology* / Q000517:prevention & control*; D002762:Cholecalciferol / Q000008:administration & dosage; D004041:Dietary Fats / Q000008:administration & dosage; D006862:Hydrogen Sulfide / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D008055:Lipids; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D002762:Cholecalciferol; D006862:Hydrogen Sulfide