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Heat shock protein 72 confers protection in retinal ganglion cells and lateral geniculate nucleus neurons via blockade of the SAPK/JNK pathway in a chronic ocular-hypertensive rat model

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Neural Regeneration Research 2014年第14期9卷 1395-1401页

作者： Ning Li Yuehua Li Xuanchu Duan Department of Ophthalmology The First Affiliated Hospital of Anhui Medical University Department of Ophthalmology Second Xiangya HospitalCentral South University

Optic nerve transection increased the expression of heat shock protein 72 （HSP72） in the lateral geniculate body, indicating that this protein is involved in the prevention of neuronal injury. Zinc sulfate and quercetin induced and inhibited the expression of HSP72, respectively. Intraperitoneal injections of zinc sulfate, SP600125 （c-Jun N-terminal kinase inhibitor）, or quercetin were performed on retinal ganglion cells in a Wistar rat model of chronic ocular hypertension. Our results showed that compared with the control group, the expression of HSP72 in retinal ganglion cells and the lateral geniculate body was increased after the injection of zinc sulfate, but was decreased after the injection of quercetin. The expression of phosphorylated c-Jun N-terminal kinases and phosphorylated c-Jun were visible 3 days after injection in the control group, and reached apeak at 7 days. Zinc sulfate and SP600125 significantly decreased the expression of p-c-Jun, whereas quercetin significantly enhanced the expression of this protein. These results suggest that HSP72 protects retinal ganglion cells and lateral geniculate body in a rat model of chronic ocular hypertension from injury by blocking the activation of the stress-activated kinase/c-Jun N-terminal kinase apoptotic pathway.

关键词： nerve regeneration peripheral nerve injury glaucoma heat shock protein 72 retinalganglion cells lateral geniculate body zinc sulfate quercetin SAPK/JNK pathway neuroprotection p-INK p-c-Jun NSFC grant neural regeneration

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