Astragalus injection protects cerebral ischemic injury by inhibiting neuronal apoptosis and the expression of JNK3 after
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RESEARCH
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Astragalus injection protects cerebral ischemic injury by inhibiting neuronal apoptosis and the expression of JNK3 after cerebral ischemia reperfusion in rats Guangyi Liu, Jinming Song, Yunliang Guo*, Tingting Wang and Zhen Zhou
Abstract Background: Astragalus is a widely used traditional Chinese medicine and has been proven beneficial for many aspects of human health. It is important to explore the neuroprotective effect and mechanism of astragalus injection in cerebral ischemia reperfusion injury. Methods: The focal cerebral ischemic model with middle cerebral artery occlusion (MCAO) reperfusion was established by Longa’s method in healthy adult male Wistar rats, and treated by injecting intraperitoneally astragalus injection (3 ml/kg). The neurobehavioral function of rats was evaluated by Longa’s test. The cerebral blood flow (CBF) was measured by laser Doppler flowmetry and the cerebral infarct volume was calculated by tetrazolium chloride (TTC) stain. The shape and structure of neurons in parahippocampal area was observed by HE stain and the neuronal apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and flow cytometry. The expressions of c-jun N-terminal kinase 3 (JNK3) mRNA and protein were determined by RT-PCR and immunohistochemical assay and Western blotting respectively. Results: After treatment with astragalus injection, the expressions of JNK3 mRNA and protein reduced significantly, the number of neuronal apoptosis minus, the cerebral infarct volume shrink, the neuronal shape-structure and animal neurobehavioral function improved significantly than those in model rats. Conclusions: It is suggested that astragalus injection could inhibit neuronal apoptosis, reduce infarct volume and improve neurobehavioral function by down-regulating the expression of JNK3 gene after cerebral ischemia reperfusion injury in rats. Keywords: Astragalus injection, Cerebral ischemia, Reperfusion injury, Apoptosis, JNK3, Rats
Background Neuronal apoptosis in ischemic penumbra is one of the mechanisms of neuronal damage in ischemic cerebrovascular disease [1]. The c-jun amino terminal kinase (c-Jun N-terminal kinase, JNK) signaling is an important pathway of mitogen-activated protein kinase (MAPK) [2] and plays an important regulatory role in programmed cell death [3]. The encoding JNK genes found presently in mammalian cells included jnk1, jnk2 and jnk3, and their corresponding coding product JNK1 and JNK2 * Correspondence: [email protected] Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong 266003, China
expressed widely, while JNK3 expressed only in brain, heart and testicular tissues [4]. JNK3 is the key signal in neuronal apoptosis during brain ischemia [5], and the JNK3 gene knockout not only reduce the c-jun phosphorylation but also protect the brain injury caused by cerebral ischemia/hypoxia [6], so that inhibiting JNK3 expression and neuronal apoptosis maybe one of important met
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