PMID- 20476551
OWN - NLM
STAT- MEDLINE
DCOM- 20130131
LR  - 20131121
IS  - 1000-6834 (Print)
IS  - 1000-6834 (Linking)
VI  - 26
IP  - 1
DP  - 2010 Feb
TI  - [Effect of hydrogen sulfide on antiatherosclerosis in rats].
PG  - 1-7
AB  - 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. CONCLUSION: 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.
FAU - Chen, Shi-jian
AU  - Chen SJ
AD  - Department of Physiology, School of Basic Medicine, Wuhan University, China.
FAU - Yan, Xiao-hongl
AU  - Yan XH
FAU - Zhu, Xiao-yingt
AU  - Zhu XY
FAU - Hu, Min
AU  - Hu M
FAU - Hu, Sheng-guo
AU  - Hu SG
FAU - Yuan, Wen-jun
AU  - Yuan WJ
LA  - chi
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhongguo Ying Yong Sheng Li Xue Za Zhi
JT  - Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = 
      Chinese journal of applied physiology
JID - 9426407
RN  - 0 (Dietary Fats)
RN  - 0 (Lipids)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (vascular endothelial growth factor A, rat)
RN  - 1C6V77QF41 (Cholecalciferol)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/*physiopathology/*prevention & control
MH  - Cholecalciferol/administration & dosage
MH  - Dietary Fats/administration & dosage
MH  - Hydrogen Sulfide/metabolism/*pharmacology/therapeutic use
MH  - Lipids/blood
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vascular Endothelial Growth Factor A/genetics/metabolism
EDAT- 2010/05/19 06:00
MHDA- 2013/02/01 06:00
CRDT- 2010/05/19 06:00
PHST- 2010/05/19 06:00 [entrez]
PHST- 2010/05/19 06:00 [pubmed]
PHST- 2013/02/01 06:00 [medline]
PST - ppublish
SO  - Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2010 Feb;26(1):1-7.