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5'-adenosine monophosphate-induced hypothermia attenuates brain ischemia/reperfusion injury in a rat model by inhibiting the inflammatory response.

Miao YF, Wu H, Yang SF, Dai J, Qiu YM, Tao ZY, Zhang XH - Mediators Inflamm. (2015)

Bottom Line: Hypothermia treatment is a promising therapeutic strategy for brain injury.Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls.AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Ren Ji Hospital, South Campus, Shanghai Jiao Tong University School of Medicine, Shanghai 201112, China.

ABSTRACT
Hypothermia treatment is a promising therapeutic strategy for brain injury. We previously demonstrated that 5'-adenosine monophosphate (5'-AMP), a ribonucleic acid nucleotide, produces reversible deep hypothermia in rats when the ambient temperature is appropriately controlled. Thus, we hypothesized that 5'-AMP-induced hypothermia (AIH) may attenuate brain ischemia/reperfusion injury. Transient cerebral ischemia was induced by using the middle cerebral artery occlusion (MCAO) model in rats. Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls. AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells. The overall infarct volume was significantly smaller in AIH-treated rats, and neurological function was improved. By contrast, rats with ischemic brain injury that were administered 5'-AMP without inducing hypothermia had ischemia/reperfusion injuries similar to those in euthermic controls. Thus, the neuroprotective effects of AIH were primarily related to hypothermia.

No MeSH data available.


Related in: MedlinePlus

AIH inhibits neuronal apoptosis in the infarcted brain. (a–e) Fluorescence results of the TUNEL assay in the sham, MCAO, NT, HT(1.0), and HT(0.5) groups. Bright green dots were deemed apoptotic cells. Scale bar = 50 μm. (f) Quantitative analysis of apoptotic cells 24 h after ischemia. TUNEL-positive cells were counted from 3 random 1 × 1 mm2 areas. All values are the mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
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fig4: AIH inhibits neuronal apoptosis in the infarcted brain. (a–e) Fluorescence results of the TUNEL assay in the sham, MCAO, NT, HT(1.0), and HT(0.5) groups. Bright green dots were deemed apoptotic cells. Scale bar = 50 μm. (f) Quantitative analysis of apoptotic cells 24 h after ischemia. TUNEL-positive cells were counted from 3 random 1 × 1 mm2 areas. All values are the mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.

Mentions: TUNEL staining was used to explore apoptosis in the infarcted area. Brains from rats in the MCAO, NT, and HT(0.5) groups displayed significant numbers of TUNEL-positive nuclei (bright green fluorescence) compared to the sham group (Figures 4(a), 4(b), 4(c), and 4(e)). The number of TUNEL-positive nuclei in the infarcted brains from the HT(1.0) group was reduced to 10.68% of the level observed in the MCAO group (Figure 4(d)). Quantitative analysis indicated that AIH treatment significantly inhibited apoptosis in the infarcted brain area compared to the MCAO, NT, and HT(0.5) groups (P < 0.05, Figure 4(f)).


5'-adenosine monophosphate-induced hypothermia attenuates brain ischemia/reperfusion injury in a rat model by inhibiting the inflammatory response.

Miao YF, Wu H, Yang SF, Dai J, Qiu YM, Tao ZY, Zhang XH - Mediators Inflamm. (2015)

AIH inhibits neuronal apoptosis in the infarcted brain. (a–e) Fluorescence results of the TUNEL assay in the sham, MCAO, NT, HT(1.0), and HT(0.5) groups. Bright green dots were deemed apoptotic cells. Scale bar = 50 μm. (f) Quantitative analysis of apoptotic cells 24 h after ischemia. TUNEL-positive cells were counted from 3 random 1 × 1 mm2 areas. All values are the mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig4: AIH inhibits neuronal apoptosis in the infarcted brain. (a–e) Fluorescence results of the TUNEL assay in the sham, MCAO, NT, HT(1.0), and HT(0.5) groups. Bright green dots were deemed apoptotic cells. Scale bar = 50 μm. (f) Quantitative analysis of apoptotic cells 24 h after ischemia. TUNEL-positive cells were counted from 3 random 1 × 1 mm2 areas. All values are the mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
Mentions: TUNEL staining was used to explore apoptosis in the infarcted area. Brains from rats in the MCAO, NT, and HT(0.5) groups displayed significant numbers of TUNEL-positive nuclei (bright green fluorescence) compared to the sham group (Figures 4(a), 4(b), 4(c), and 4(e)). The number of TUNEL-positive nuclei in the infarcted brains from the HT(1.0) group was reduced to 10.68% of the level observed in the MCAO group (Figure 4(d)). Quantitative analysis indicated that AIH treatment significantly inhibited apoptosis in the infarcted brain area compared to the MCAO, NT, and HT(0.5) groups (P < 0.05, Figure 4(f)).

Bottom Line: Hypothermia treatment is a promising therapeutic strategy for brain injury.Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls.AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Ren Ji Hospital, South Campus, Shanghai Jiao Tong University School of Medicine, Shanghai 201112, China.

ABSTRACT
Hypothermia treatment is a promising therapeutic strategy for brain injury. We previously demonstrated that 5'-adenosine monophosphate (5'-AMP), a ribonucleic acid nucleotide, produces reversible deep hypothermia in rats when the ambient temperature is appropriately controlled. Thus, we hypothesized that 5'-AMP-induced hypothermia (AIH) may attenuate brain ischemia/reperfusion injury. Transient cerebral ischemia was induced by using the middle cerebral artery occlusion (MCAO) model in rats. Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls. AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells. The overall infarct volume was significantly smaller in AIH-treated rats, and neurological function was improved. By contrast, rats with ischemic brain injury that were administered 5'-AMP without inducing hypothermia had ischemia/reperfusion injuries similar to those in euthermic controls. Thus, the neuroprotective effects of AIH were primarily related to hypothermia.

No MeSH data available.


Related in: MedlinePlus