Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · 2015
[Enhanced expression of Toll-like receptor 3 in the basilar arteries and hippocampus of subarachnoid hemorrhage rats].
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Xing Wenli, Tan Guanping, He Chaohui
Аннотация
OBJECTIVE: To observe the dynamic expression and significance of Toll-like receptor 3 (TLR3) in subarachnoid hemorrhage (SAH) model.
METHODS: SAH model was established using blood injection into the prechiasmatic cistern. Sixty SD rats were randomly divided into sham group and SAH groups (including SAH 1-, 3-, 7-day groups), each with 15 rats. The operation steps were the same in groups except the sham group that was injected with normal saline instead. At different time points after modeling, the basilar arteries and brain were obtained. The mRNA and protein expression of TLR3 was detected using reverse transcription PCR, Western blotting and immunohistochemistry, respectively. Meanwhile, the distribution of TLR3 was analyzed using the immunofluorescence double labeling technique.
RESULTS: The mRNA and protein expression of TLR3 was weak in sham group and highly expressed in SAH groups, and the highest expression were found in SAH 3-day group. Immunohistochemistry showed that TLR3 was highly expressed in vascular endothelial and hippocampal neurons. The sham group showed a weak TLR3 expression in the cytoplasm, while the SHA group showed the strongly expressed TLR3 mainly in the nucleus and cytoplasm. The result of immunofluorescence double labeling also suggested TLR3 was co-localization with CD34 in the endothelial cells.
CONCLUSION: The TLR3 expression was enhanced in the basilar arteries and hippocampus when the rats suffered from SAH, which suggested TLR3 might play a certain role in the pathogenesis of SAH.
METHODS: SAH model was established using blood injection into the prechiasmatic cistern. Sixty SD rats were randomly divided into sham group and SAH groups (including SAH 1-, 3-, 7-day groups), each with 15 rats. The operation steps were the same in groups except the sham group that was injected with normal saline instead. At different time points after modeling, the basilar arteries and brain were obtained. The mRNA and protein expression of TLR3 was detected using reverse transcription PCR, Western blotting and immunohistochemistry, respectively. Meanwhile, the distribution of TLR3 was analyzed using the immunofluorescence double labeling technique.
RESULTS: The mRNA and protein expression of TLR3 was weak in sham group and highly expressed in SAH groups, and the highest expression were found in SAH 3-day group. Immunohistochemistry showed that TLR3 was highly expressed in vascular endothelial and hippocampal neurons. The sham group showed a weak TLR3 expression in the cytoplasm, while the SHA group showed the strongly expressed TLR3 mainly in the nucleus and cytoplasm. The result of immunofluorescence double labeling also suggested TLR3 was co-localization with CD34 in the endothelial cells.
CONCLUSION: The TLR3 expression was enhanced in the basilar arteries and hippocampus when the rats suffered from SAH, which suggested TLR3 might play a certain role in the pathogenesis of SAH.