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OBJECTIVE: To observe the influence of scalp acupuncture on cerebral infarct size and expression of IL-10, IL-6, and IL-1β in the para-hippocampal gyrus in acute ischemic cerebrovascular disease(AICD) rats, so as to investigate its mechanisms underlying improvement of AICD. METHODS: Forty-eight male SD rats were randomly allocated to normal control (control), AICD model, medication, and scalp acupuncture groups (n＝12 per group). The AICD model was established by occlusion of the middle cerebral artery (MCAO). Rats of the medication group received intraperitoneal injection of Ammonium 1-Pyrrolidinedithiocarbamate (APDC, 100 mg•kg－1•d－1), once daily for 7 days. Scalp acupuncture stimulation was applied to bilateral "Dingnieqianxiexian" (MS6) once daily for 7 days. Before and after intervention, the neurologic deficit score (NDS) and the neurological score (NS) were evaluated according to Longa's and Schäbitz's methods, respectively. At the end of the intervention, the para-hippocampal gyrus and whole brain were collected respectively. The expression levels of IL-10, IL-6 and IL-1β in the para-hippocampal gyrus tissue were detected by immunohistochemistry, and the cerebral infarct volume of the brain was detected by triphenyltetrazollium chloride (TTC) staining after sectioning. RESULTS: Following modeling, the NDS, NS and the expression of IL-10, IL-6 and IL-1β in para-hippocampal gyrus were significantly increased in the model group compared with the control group (P0.05). The effect of scalp acupuncture was obviously superior to that of medication in up-regulating IL-10 expression level (P0.05). CONCLUSION: Scalp acupuncture can improve neurological function and reduce infarct volume in AICD rats, which may be associated with its function in up-regulating the expression of IL-10 and in inhibiting the expression of IL-6 and IL-1β to reduce inflammation reaction.
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OBJECTIVE: To observe the effect of acupuncture on the expression of silent information regulator factor 2-related enzyme 1 (SIRT 1) and nuclear factor-κB (NF-κB) in rats with acute cerebral ischemia (ACI), so as to explore its mechanisms underlying improvement of ACI. METHODS: One hundred female SD rats were randomly divided into 5 groups: normal control (normal), sham-operation (sham), model, non-acupoint and acupoint, with 20 rats in each. The ACI model was established by occlusion (electric coagulation) of the middle cerebral artery after craniotomy. "Baihui" (GV 20) and "Shuigou" (GV 26) or non-acupoints were punctured with filiform needles which were retained for 30 min after rotating for 1 min. The treatment was conducted once after modeling and 24 h thereafter. The cerebral infarct volume was measured after 2,3,5-triphenyltetrazolium chloride (TTC) staining. The contents of interleukin-1 β (IL-1 β), IL-6 and IL-8 in the serum and ischemic brain tissue were detected by radioimmunoassay, and the expression of protein SIRT 1 and NF-κB p 65 in the ischemic brain tissue was detected by immunoblotting. RESULTS: The brain infarction volume was obvious in the model group in comparison with the normal group (P0.05). CONCLUSION: Acupuncture intervention at acupoints can reduce the ischemic infarction volume in ACI rats, which may be associated with its effects in down-regulating the levels of IL-1 β, IL-6 and IL-8 in the serum and ischemic brain tissue, and in regulating cerebral SIRT 1/NF-κB signaling.
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<p><b>OBJECTIVE</b>To explore the effect of electroacupuncture(EA) preconditioning on cerebral infarct volume and the contents of TNF-α, IL-10 in serum of rats with cerebral ischemia-reperfusion injury.</p><p><b>METHODS</b>Thirty-six rats were randomly divided into a sham operation group, a model group and an EA preconditioning group, 12 rats in each group, which were further divided into 12 h and 24 h after reperfusion subgroups, 6 rats in each one. EA was used before model establishment for 2 weeks in the EA preconditioning group. The model of cerebral ischemia-reperfusion injury in rats was established with modified Longa suture method. 12 h and 24 h after reperfusion, the degree of neurological deficit was assessed by the modified behavioral scoring scale; the cerebral infarct volume was measured by TTC method and the contents of TNF-α, IL-10 in serum were detected by ELISA method.</p><p><b>RESULTS</b>Compared with the model group, the neurological severity scores in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both<0.05), the cerebral infarct volume in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both<0.05). Compared with the sham operation group, the serum TNF-α, IL-10 contents in the model group increased 12 h and 24 h after reperfusion (both<0.05). Compared with the model group, the serum TNF-α content reduced, while the serum IL-10 content increased in the EA preconditioning group 12 h after reperfusion (both<0.05). Compared with the model group, the serum TNF-α, IL-10 contents reduced in the EA preconditioning group 24 h after reperfusion (both<0.05).</p><p><b>CONCLUSION</b>EA preconditioning can improve neurological deficit, reduce cerebral infarct volume after cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the regulation of EA on the dynamic balance between pro-inflammatory cytokine TNF-α and anti-inflammatory cytokine IL-10 in peripheral blood of cerebral ischemia-reperfusion injury in acute phase, thus alleviate acute cerebral ischemia-reperfusion inflammatory response.</p>
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Objective To investigate the influence of Buyanghuanwu (BYHW) Decoction on cerebral infarct volume and pathological changes after cerebral ischemia and reperfusion. Methods The model of focal cerebral ischemia and reperfusion was made by thread embolism method. Healthy male SD rats were divided randomly into sham-operated group, model group and BYHW Decoction group. Infarct volume was detected by triphenyltetrazolium chloride (TTC) staining and pathological changes were observed microscopically in HE stained sections. Results In BYHW Decoction group, infarct volume was significantly smaller than that in model group (P