04 January 2020 : Animal Research
Protective Effects of Naringin in Cerebral Infarction and Its Molecular MechanismJinping Yang1ABCDEFG*, Lei Yuan1ABCDEFG, Ying Wen1BCD, Haiyan Zhou1BCD, Wenhan Jiang1BC, Dan Xu1CDE, Minling Wang1ABEF
Med Sci Monit 2020; 26:e918772
BACKGROUND: Cerebral infarction is a cardiovascular disease with high morbidity and mortality. At present, many studies have reported the treatment of cerebral infarction by traditional Chinese medicine. Naringin, a flavonoid, is a major traditional Chinese medicine. However, the effect and mechanism of naringin on cerebral infarction is unclear.
MATERIAL AND METHODS: In our study, we established a rat model of cerebral infarction through middle cerebral artery occlusion (MCAO) to study the influence of naringin on cerebral infarction in vivo. After treatment with naringin, brain water content was detected to assess brain edema. Cerebral infarction volume and neurological deficits were also measured. Production of the inflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-6) was measured using enzyme-linked immunosorbent assay (ELISA). Besides, the effect of naringin on cerebral infarction was investigated in vitro by establishing an oxygen-glucose deprivation (OGD) model in neuronal cells. Cell apoptosis and cell viability was determined using flow cytometry and MTT assay.
RESULTS: We found that naringin pretreatment significantly decreased the brain water content, cerebral infarction volume, and neurological deficit scores of MCAO subjected rats. And naringin treatment reduced apoptosis of nerve cells in rat hippocampus and the secretion of inflammatory factor such as TNF-α and IL-6. Besides, we found that naringin increased cell viability and inhibited apoptosis in OGD induced neuronal cells. Finally, we found that naringin promoted the expression of p-AKT protein in a concentration-dependent manner and activated the PI3K/AKT pathway in OGD induced neurons.
CONCLUSIONS: Naringin played a protective role in cerebral infarction via suppressing neuronal apoptosis and inflammation.
Keywords: cerebral infarction, Infarction, Middle Cerebral Artery, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Brain, Brain Ischemia, Flavanones, Hippocampus, Interleukin-6, Neurons, Neuroprotective Agents
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