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Upregulated expression of S100A8 in mice brain after focal cerebral ischemia reperfusion.

Sun P, Li Q, Zhang Q, Xu L, Han JY - World J Emerg Med (2013)

Bottom Line: Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores.The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Emergency Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

ABSTRACT

Background: Recent studies have showed that S100A8 has been implicated in the pathobiology of inflammatory disorders, and that cerebral ischemia reperfusion (I/R) rapidly activates inflammation responses via Toll-like receptor 4 (TLR4). This study aimed to explore the expression of S100A8 and the relationship between S100A8 and TLR4 in focal cerebral ischemia reperfusion injury.

Methods: C3H/HeJ mice (n=30) and C3H/HeN mice (n=30) were divided randomly into a C3H/HeJ model group (n=18), a C3H/HeJ control group (n=12), a C3H/HeN model group (n=18), and a C3H/HeN control group (n=12). Middle cerebral artery I/R model in mice was produced using a thread embolism method. The brains of the mice were collected after ischemia for 1 hour and reperfusion for 12 hours. Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores. Brain injury after cerebral I/R was observed by an optical microscope after TTC and HE dyeing. The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.

Results: Compared with C3H/HeN mice, TLR4-deficient mice (C3H/HeJ) had lower infarct volumes and better outcomes in neurological tests. The levels of S100A8 increased sharply in the brains of mice after I/R injury. In addition, mice that lacked TLR4 (C3H/HeJ) had lower expression of I/R-induced S100A8 than C3H/HeN mice in the model group, indicating that a close relationship might exist between the levels of S100A8 and TLR4.

Conclusion: S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

No MeSH data available.


Related in: MedlinePlus

Expression of S100A8 protein in the ischemic mouse brain (magnification×400). A: C3H/HeN control group; B: C3H/HeN model group; C: C3H/HeJ control group; D: C3H/HeJ model group.
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Figure 2: Expression of S100A8 protein in the ischemic mouse brain (magnification×400). A: C3H/HeN control group; B: C3H/HeN model group; C: C3H/HeJ control group; D: C3H/HeJ model group.


Upregulated expression of S100A8 in mice brain after focal cerebral ischemia reperfusion.

Sun P, Li Q, Zhang Q, Xu L, Han JY - World J Emerg Med (2013)

Expression of S100A8 protein in the ischemic mouse brain (magnification×400). A: C3H/HeN control group; B: C3H/HeN model group; C: C3H/HeJ control group; D: C3H/HeJ model group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4129849&req=5

Figure 2: Expression of S100A8 protein in the ischemic mouse brain (magnification×400). A: C3H/HeN control group; B: C3H/HeN model group; C: C3H/HeJ control group; D: C3H/HeJ model group.
Bottom Line: Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores.The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Emergency Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

ABSTRACT

Background: Recent studies have showed that S100A8 has been implicated in the pathobiology of inflammatory disorders, and that cerebral ischemia reperfusion (I/R) rapidly activates inflammation responses via Toll-like receptor 4 (TLR4). This study aimed to explore the expression of S100A8 and the relationship between S100A8 and TLR4 in focal cerebral ischemia reperfusion injury.

Methods: C3H/HeJ mice (n=30) and C3H/HeN mice (n=30) were divided randomly into a C3H/HeJ model group (n=18), a C3H/HeJ control group (n=12), a C3H/HeN model group (n=18), and a C3H/HeN control group (n=12). Middle cerebral artery I/R model in mice was produced using a thread embolism method. The brains of the mice were collected after ischemia for 1 hour and reperfusion for 12 hours. Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores. Brain injury after cerebral I/R was observed by an optical microscope after TTC and HE dyeing. The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.

Results: Compared with C3H/HeN mice, TLR4-deficient mice (C3H/HeJ) had lower infarct volumes and better outcomes in neurological tests. The levels of S100A8 increased sharply in the brains of mice after I/R injury. In addition, mice that lacked TLR4 (C3H/HeJ) had lower expression of I/R-induced S100A8 than C3H/HeN mice in the model group, indicating that a close relationship might exist between the levels of S100A8 and TLR4.

Conclusion: S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

No MeSH data available.


Related in: MedlinePlus