【摘要】：目的研究腺苷A2A受體阻斷劑對大鼠氯化鋰-毛果蕓香堿癲癇持續(xù)狀態(tài)(SE)模型的影響。方法選取50只WD大鼠隨機分為對照組、模型組及A2A受體阻斷劑組。模型組采用氯化鋰-毛果蕓香堿腹腔注射復(fù)制癲癇模型,A2 A受體阻斷劑組在氯化鋰-毛果蕓香堿注射前15 min予腹腔給藥(SCH58261 0.05 mg/kg),對照組給予同等劑量生理鹽水。在成功誘導(dǎo)癲癇發(fā)作40 min后予地西泮及水合氯醛終止發(fā)作,并于發(fā)作終止后24 h留取標(biāo)本。尼氏染色法檢測三組中海馬神經(jīng)元損傷情況,Westernblot法檢測MAPKs(JNK/p-JNK、P38/p-P38和ERK/p-ERK)表達變化。結(jié)果對照組、模型組及A2A受體阻斷劑組雙側(cè)海馬CA3區(qū)正常形態(tài)神經(jīng)元計數(shù)分別為158.6±8.4、59.8±7.4和123.4±5.0,模型組神經(jīng)元計數(shù)顯著低于對照組,差異具有統(tǒng)計學(xué)意義(P0.05),A2A受體阻斷劑組神經(jīng)元計數(shù)顯著高于模型組,差異具有統(tǒng)計學(xué)意義(P0.05)。Westernblot法檢測顯示p-JNK、p-P38和p-ERK在模型組中表達明顯增多,在A2A受體阻斷劑組中p-JNK和p-P38表達減少。結(jié)論氯化鋰-毛果蕓香堿模型中,腺苷A2A受體阻斷劑可能通過抑制p-JNK他p-P38的表達對神經(jīng)元損傷起到保護作用。
[Abstract]:Aim to study the effect of adenosine A 2A receptor blocker on (SE) model of lithium-pilocarpine epileptic status in rats. Methods 50 WD rats were randomly divided into control group, model group and A 2A receptor blocker group. The model group was treated with lithium-pilocarpine intraperitoneal injection and the control group was given intraperitoneal administration of lithium-pilocarpine (SCH58261 0.05 mg/kg) 15 min before the injection of lithium-pilocarpine, and the control group was given the same dose of normal saline. Diazepam and chloral hydrate were given to the epileptic seizure for 40 min and the specimens were collected 24 hours after the seizure was successfully induced. The expression of MAPKs (JNKP / p-JNKP38 / p-P38 and ERK/p-ERK) was detected by Western blot in the three groups. Results the number of normal neurons in the bilateral hippocampal CA3 region in the control group, model group and A2A receptor blocker group was 158.6 鹵8.4 鹵59.8 鹵7.4 and 123.4 鹵5.0, respectively. The number of neurons in the model group was significantly lower than that in the control group. The difference was statistically significant (P0.05) the number of neurons in the A2A receptor blocker group was significantly higher than that in the model group. The difference was statistically significant (P0.05) .Western blot analysis showed that the expression of p-JNKN p-P38 and p-ERK in the model group was significantly increased, and the expression of p-JNK and p-P38 in the A2A receptor blocker group was decreased. Conclusion in lithium-pilocarpine model, adenosine A 2A receptor antagonist may play a protective role in neuronal injury by inhibiting the expression of p-JNK p-P38.
【作者單位】： 廣東省深圳市南山區(qū)人民醫(yī)院神經(jīng)內(nèi)科;華中科技大學(xué)附屬同濟醫(yī)院神經(jīng)內(nèi)科;
【基金】：國家自然科學(xué)基金青年基金項目(81201006) 深圳市南山區(qū)技術(shù)研發(fā)和創(chuàng)意設(shè)計項目分項基金(南科研衛(wèi)2012002;南科研衛(wèi)2014015)
【分類號】：R-332;R742.1

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