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Rosiglitazone protects against severe hemorrhagic shock-induced organ damage in rats.

Yang FL, Subeq YM, Lee CJ, Lee RP, Peng TC, Harn HJ, Hsu BG - Med. Sci. Monit. (2011)

Bottom Line: The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect.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.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Tzu Chi University, Hualien, Taiwan.

ABSTRACT

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.

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Related in: MedlinePlus

Change in serum glutamic oxaloacetic transaminase (GOT) (A), glutamic pyruvic transaminase (GPT) (B), blood urea nitrogen (BUN) (C) and creatinine (Cre) (D) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
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f2-medscimonit-17-10-br282: Change in serum glutamic oxaloacetic transaminase (GOT) (A), glutamic pyruvic transaminase (GPT) (B), blood urea nitrogen (BUN) (C) and creatinine (Cre) (D) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.

Mentions: GOT was gradually increased after induction of HS (Figure 2A). Compared with the HS group, treatment with rosiglitazone decreased GOT at 3, 6, 9, and 12 h after induction of HS (#P<0.05; Figure 2A). Serum GPT increased at 0, 1, 3, 6, 9, and 12 h after HS compared with the Control group (*P < 0.05; Figure 2B). Compared with the HS group, treatment with rosiglitazone decreased the GPT at 3, 6, 9, and 12 h (#P<0.05; Figure 2B). The GOT and GPT were no statistically different between the Rosiglitazone group and the Control group.


Rosiglitazone protects against severe hemorrhagic shock-induced organ damage in rats.

Yang FL, Subeq YM, Lee CJ, Lee RP, Peng TC, Harn HJ, Hsu BG - Med. Sci. Monit. (2011)

Change in serum glutamic oxaloacetic transaminase (GOT) (A), glutamic pyruvic transaminase (GPT) (B), blood urea nitrogen (BUN) (C) and creatinine (Cre) (D) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539481&req=5

f2-medscimonit-17-10-br282: Change in serum glutamic oxaloacetic transaminase (GOT) (A), glutamic pyruvic transaminase (GPT) (B), blood urea nitrogen (BUN) (C) and creatinine (Cre) (D) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
Mentions: GOT was gradually increased after induction of HS (Figure 2A). Compared with the HS group, treatment with rosiglitazone decreased GOT at 3, 6, 9, and 12 h after induction of HS (#P<0.05; Figure 2A). Serum GPT increased at 0, 1, 3, 6, 9, and 12 h after HS compared with the Control group (*P < 0.05; Figure 2B). Compared with the HS group, treatment with rosiglitazone decreased the GPT at 3, 6, 9, and 12 h (#P<0.05; Figure 2B). The GOT and GPT were no statistically different between the Rosiglitazone group and the Control group.

Bottom Line: The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect.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.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Tzu Chi University, Hualien, Taiwan.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus