Purpose:To investigate the dynamics of heat shock protein 72(HSP72) expression in retinal ganglion cells(RGCs) in rat model of acute glaucoma treated with heat stress or intraperitoneal injection of zinc sulfate.Metho...Purpose:To investigate the dynamics of heat shock protein 72(HSP72) expression in retinal ganglion cells(RGCs) in rat model of acute glaucoma treated with heat stress or intraperitoneal injection of zinc sulfate.Methods:Twenty-seven male Wistar rats were used to make acute glaucoma models. Five others served as normal control. Acute glaucoma models were made by intracameral irrigation in the right eyes with balanced salt saline (BSS) at 102 mmHg for 2 hours. Nine model rats were killed at different intervals after intracameral irrigation without treatment,which served as damage control. Ten were treated with heat stress 40℃～42℃, and 8 were used for zinc sulfate administration 2 days posterior to intracameral irrigation. Treated model rats were sacrificed at designed intervals after treatment. Right eyes were enucleated immediately, and the retinas were dissected for Western blot.Results:No HSP72 was found in RGCs of normal Wistar rats. In damage control group, slight HSP72 was detected during 6～36 hours posterior to intracameral irrigation. HSP72 was detected significantly expressed in RGCs of both heat shock group and zinc sulfate group. But the dynamics of HSP72 production were quite different in these two treated groups. In heat shock group, HSP72 appeared at the sixth hour after treatment, and increased gradually until its peak production emerged at the 48th hour. HSP72 vanished 8 days later after treatment. In zinc sulfate group, HSP72 expression began 24 hours later after zinc administration, and reached its highest level at the 72th hour posterior to treatment. HSP72 expression then decreased slowly, and disappeared 21 days later after treatment. Conclusion:HSP72 can be induced in RGCs of rat acute glaucoma models with heat stress or zinc sulfate adddministration. But the dynamics of the HSP72 induction in those two groups were quite different. Eye Science 2004;20:30-33.展开更多
Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role ...Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role of theγ-hydroxybutyrate analog HOCPCA in a glaucoma model,focusing on its effects on CaMKII signaling,oxidative stress,and neuroinflammatory responses.Retinal tissue from high IOP animal models was analyzed via proteomics.In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress,followed by HOCPCA treatment.HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure,preserving neuronal function.It restored CaMKIIαandβlevels,preserving RGC integrity,while also modulating oxidative stress and neuroinflammatory responses.These findings suggest that HOCPCA,through its interaction with CaMKII,holds promise as a neuroprotective therapy for glaucoma.展开更多
文摘Purpose:To investigate the dynamics of heat shock protein 72(HSP72) expression in retinal ganglion cells(RGCs) in rat model of acute glaucoma treated with heat stress or intraperitoneal injection of zinc sulfate.Methods:Twenty-seven male Wistar rats were used to make acute glaucoma models. Five others served as normal control. Acute glaucoma models were made by intracameral irrigation in the right eyes with balanced salt saline (BSS) at 102 mmHg for 2 hours. Nine model rats were killed at different intervals after intracameral irrigation without treatment,which served as damage control. Ten were treated with heat stress 40℃～42℃, and 8 were used for zinc sulfate administration 2 days posterior to intracameral irrigation. Treated model rats were sacrificed at designed intervals after treatment. Right eyes were enucleated immediately, and the retinas were dissected for Western blot.Results:No HSP72 was found in RGCs of normal Wistar rats. In damage control group, slight HSP72 was detected during 6～36 hours posterior to intracameral irrigation. HSP72 was detected significantly expressed in RGCs of both heat shock group and zinc sulfate group. But the dynamics of HSP72 production were quite different in these two treated groups. In heat shock group, HSP72 appeared at the sixth hour after treatment, and increased gradually until its peak production emerged at the 48th hour. HSP72 vanished 8 days later after treatment. In zinc sulfate group, HSP72 expression began 24 hours later after zinc administration, and reached its highest level at the 72th hour posterior to treatment. HSP72 expression then decreased slowly, and disappeared 21 days later after treatment. Conclusion:HSP72 can be induced in RGCs of rat acute glaucoma models with heat stress or zinc sulfate adddministration. But the dynamics of the HSP72 induction in those two groups were quite different. Eye Science 2004;20:30-33.
基金The position of M.H.was funded by grants from the state of North-Rhine-Westphalia,Germany(AZ:323-8.04.10.02-141905)the German Center for Infection Research,DZIF(TTU 08.927 and TTU 08.928)+1 种基金the Deutsche Forschungsgemeinschaft(DFG),SFB 670 procured by Prof.Dr.Martin Krönkesupported by the Deutsche Forschungsgemeinschaft(DFG)with grants PR1569/1-1 and PR 1569/1-3.
文摘Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role of theγ-hydroxybutyrate analog HOCPCA in a glaucoma model,focusing on its effects on CaMKII signaling,oxidative stress,and neuroinflammatory responses.Retinal tissue from high IOP animal models was analyzed via proteomics.In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress,followed by HOCPCA treatment.HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure,preserving neuronal function.It restored CaMKIIαandβlevels,preserving RGC integrity,while also modulating oxidative stress and neuroinflammatory responses.These findings suggest that HOCPCA,through its interaction with CaMKII,holds promise as a neuroprotective therapy for glaucoma.
