mTOR/autophagy pathway in the hippocampus of rats suffering intermittent hypoxia preconditioning and global cerebral ischemia-reperfusion.
We explored the role of mTOR/autophagy pathway in the aggravation of cerebral ischemia-reperfusion nerve injury caused by intermittent hypoxia. Eighty male wistar rats were divided into four groups by the random number method: sham operation group (SO group, n=20), cerebral ischemia-reperfusion group (I/R group, n=20), intermittent hypoxia and cerebral ischemia-reperfusion group (IH+I/R group, n=20), intermittent hypoxia and cerebral ischemia-reperfusion group plus mTOR inhibitor group (inhibitor group, n=20).The results showed that compared with the SO group, HE staining showed structural damage of neurons at each time point, the immunohistochemical assay showed an increasing number of mTOR and beclin1 immune-positive cells (P<0.05) and RT-PCR showed enhanced expression of mTOR and beclin1 protein in the I/R group (P<0.05). Compared with the I/R group, HE staining showed exacerbating structural damage of neurons at each time point, the immunohistochemical assay showed an increasing number of mTOR and beclin1 immune-positive cells (P<0.05) and RT-PCR showed enhanced expression of mTOR and beclin1 protein in the IH+I/R group (P<0.05). Compared with the IH+I/R group, HE staining showed remissive structural damage of neurons at each time point, the immunohistochemical assay showed a decreasing number of mTOR immune-positive cells and a rising number of beclin1immune-positive cells (P<0.05) and RT-PCR showed weakened expression of mTOR protein and enhanced expression of beclin1 protein in the inhibitor group (P<0.05). Thence, the present study indicated that intermittent hypoxia preconditioning can aggravate the nerve injury of the global cerebral ischemia-reperfusion model, and the mechanism is associated with the activation of mTOR/autophagy pathway.
Nursing and Rehabilitation College, North China University of Science and Technology, 063000, China.
Ya-Ning
YN
Zhao
Nursing and Rehabilitation College, North China University of Science and Technology, 063000, China.
Xiang-Fei
XF
Guo
The Neurosurgery of Affiliated Hospital, North China University of Science and Technology, 063000, China.
Jian-Min
JM
Li
Nursing and Rehabilitation College, North China University of Science and Technology, 063000, China.
Chang-Xiang
CX
Chen
Nursing and Rehabilitation College, North China University of Science and Technology, 063000, China.
Shu-Xing
SX
Li
The Neurosurgery of Affiliated Hospital, North China University of Science and Technology, 063000, China.
Cheng-Jing
CJ
Xu
D000818:Animals; D001343:Autophagy / Q000502:physiology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D015687:Cell Hypoxia / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D020181:Sleep Apnea, Obstructive / Q000378:metabolism* / Q000473:pathology; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*
C546843:mTOR protein, mouse; D058570:TOR Serine-Threonine Kinases
OSAHS-patterned hypoxia; autophagy; cerebral ischemia-reperfusion; mTOR