PMID- 21959602
OWN - NLM
STAT- MEDLINE
DCOM- 20120131
LR  - 20211020
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 17
IP  - 10
DP  - 2011 Oct
TI  - Rosiglitazone protects against severe hemorrhagic shock-induced organ damage in 
      rats.
PG  - BR282-9
AB  - BACKGROUND: Hemorrhagic shock (HS) followed by resuscitation can induce the 
      production of several inflammatory mediators and lead to multiple organ 
      dysfunction. The molecular mechanism of biologic responses to rosiglitazone has 
      an anti-inflammatory effect. The present study was designed to investigate the 
      effects of rosiglitazone on physiopathology and inflammatory mediators after HS 
      in rats. MATERIAL/METHODS: HS was induced in rats by withdrawing 60% of the total 
      blood volume from a femoral artery catheter, immediately followed by intravenous 
      injection of 0.3 mg/kg rosiglitazone. Mean arterial pressure (MAP) and heart rate 
      (HR) were monitored continuously for 12 h. Levels of biochemical parameters, 
      including GOT, GPT, BUN, Cre, LDH, CPK, and lactate were measured at 30 min 
      before induction of HS and 0, 1, 3, 6, 9, and 12 h after HS, while an equal 
      volume of normal saline was replaced as fluid resuscitation. Inflammatory 
      mediators, including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 
      (IL-6) and monocyte chemoattractant protein-1 (MCP-1), were measured in serum at 
      1 and 12 h after HS. The kidneys, liver, lungs, and small intestine were removed 
      for histological assessment by hematoxylin and eosin stained at 48 h after HS. 
      RESULTS: HS significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, 
      glucose, TNF-alpha, IL-6 and MCP-1 levels, induced tachycardia, and decreased 
      mean arterial pressure (MAP) in rats. Treatment with rosiglitazone improved 
      survival rate, decreased the markers of organ injury, and suppressed the release 
      of TNF-alpha, IL-6, and MCP-1 after HS in rats. CONCLUSIONS: Treatment with 
      rosiglitazone suppresses the release of serum TNF-alpha, IL-6 and MCP-1, and 
      ameliorates HS-induced organ damage in rats.
FAU - Yang, Fwu-Lin
AU  - Yang FL
AD  - School of Medicine, Tzu Chi University, Hualien, Taiwan.
FAU - Subeq, Yi-Maun
AU  - Subeq YM
FAU - Lee, Chung-Jen
AU  - Lee CJ
FAU - Lee, Ru-Ping
AU  - Lee RP
FAU - Peng, Tai-Chu
AU  - Peng TC
FAU - Harn, Horng-Jyh
AU  - Harn HJ
FAU - Hsu, Bang-Gee
AU  - Hsu BG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Thiazolidinediones)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 05V02F2KDG (Rosiglitazone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Blood Chemical Analysis
MH  - Blood Pressure
MH  - Chemokine CCL2/blood
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Heart Rate
MH  - Interleukin-6/blood
MH  - Multiple Organ Failure/etiology/*physiopathology/*prevention & control
MH  - Rats
MH  - Rats, Wistar
MH  - Rosiglitazone
MH  - Shock, Hemorrhagic/*complications
MH  - Survival Analysis
MH  - Thiazolidinediones/*pharmacology
MH  - Tumor Necrosis Factor-alpha/blood
PMC - PMC3539481
EDAT- 2011/10/01 06:00
MHDA- 2012/02/01 06:00
PMCR- 2011/10/01
CRDT- 2011/10/01 06:00
PHST- 2011/10/01 06:00 [entrez]
PHST- 2011/10/01 06:00 [pubmed]
PHST- 2012/02/01 06:00 [medline]
PHST- 2011/10/01 00:00 [pmc-release]
AID - 881975 [pii]
AID - 10.12659/msm.881975 [doi]
PST - ppublish
SO  - Med Sci Monit. 2011 Oct;17(10):BR282-9. doi: 10.12659/msm.881975.