Ling-Ling Tang1,2, Jing-Ya Ye3, Sheng-Nan Jiang3, Jie-Sheng Zheng3. 1. State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang UniversityHangzhou 310003, Zhejiang, China. 2. Collaborative Innovation Center for Diagnosis and Treatment of Infectious DiseasesHangzhou 310058, Zhejiang, China. 3. Department of Neurosurgery, The First Affiliated Hospital, College of Medicine, Zhejiang UniversityHangzhou 310003, Zhejiang, China.
Abstract
BACKGROUND: To investigate the potential protective effects of 3,4-oxo-isopropylidene-shikimic acid (ISA) on brain ischemic injury in rats. METHODS: Cell Counting Kit-8, flow cytometry, and TUNEL were used to evaluate the cell viability and the apoptosis rate in vitro and in situ. Reactive oxygen species generation was determined by DCFH-DA assay. qPCR and Western blot were used to test the molecular mechanisms related to the anti-apoptosis effects. RESULT: Protective effect of pre-conditioning of ISA on the brain injury caused by ischemia was observed. ISA treatment showed anti-apoptosis effects on isolated primary astrocytes and neurons. ROS generation was also significantly scavenged by treatment of ISA. The treatment with ISA protected astrocytes from hypoxic condition-induced apoptosis and ischemic injury. The underlying mechanisms revealed by qPCR and WB showed that the level of mRNA and protein expression of Bax, Bcl-2, and caspase-3 were significantly down-regulated by ISA treatment (P < 0.05). Pre-conditioning with ISA is beneficial in reducing the neuronal damage caused by brain ischemia. CONCLUSION: Treatment with ISA reduces apoptosis and ROS over-generation caused by ischemic injury. Pre-conditioning with ISA resulted in significantly protective effects on brain under ischemic condition.
BACKGROUND: To investigate the potential protective effects of 3,4-oxo-isopropylidene-shikimic acid (ISA) on brain ischemic injury in rats. METHODS: Cell Counting Kit-8, flow cytometry, and TUNEL were used to evaluate the cell viability and the apoptosis rate in vitro and in situ. Reactive oxygen species generation was determined by DCFH-DA assay. qPCR and Western blot were used to test the molecular mechanisms related to the anti-apoptosis effects. RESULT: Protective effect of pre-conditioning of ISA on the brain injury caused by ischemia was observed. ISA treatment showed anti-apoptosis effects on isolated primary astrocytes and neurons. ROS generation was also significantly scavenged by treatment of ISA. The treatment with ISA protected astrocytes from hypoxic condition-induced apoptosis and ischemic injury. The underlying mechanisms revealed by qPCR and WB showed that the level of mRNA and protein expression of Bax, Bcl-2, and caspase-3 were significantly down-regulated by ISA treatment (P < 0.05). Pre-conditioning with ISA is beneficial in reducing the neuronal damage caused by brain ischemia. CONCLUSION: Treatment with ISA reduces apoptosis and ROS over-generation caused by ischemic injury. Pre-conditioning with ISA resulted in significantly protective effects on brain under ischemic condition.
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