本文選題：甘草甜素 + 海人酸��； 參考：《鄭州大學(xué)》2017年碩士論文

【摘要】：背景和目的癲癇是兒童時(shí)期常見的慢性神經(jīng)系統(tǒng)疾病,70-80%的癲癇患者通過(guò)抗癲癇藥物的治療能控制癲癇的發(fā)作,但仍有20-30%左右的癲癇患者在接受規(guī)范合理的抗癲癇藥物治療后依然有發(fā)作而成為難治性癲癇。顳葉癲癇在難治癲癇中最常見,一直以來(lái)都是癲癇治療的難點(diǎn)。大量研究表明,顳葉癲癇的反復(fù)發(fā)作可致海馬區(qū)神經(jīng)元的丟失及海馬硬化,這不僅對(duì)病人的生活、工作產(chǎn)生巨大的影響,也給患者的家庭和社會(huì)造成了很大的負(fù)擔(dān)。目前的抗癲癇藥物主要作用于離子通道,抑制神經(jīng)元的興奮性,進(jìn)行對(duì)癥治療。深入研究癲癇的病因和發(fā)病機(jī)制,針對(duì)發(fā)作機(jī)制中的關(guān)鍵環(huán)節(jié)發(fā)現(xiàn)新藥物、尋求新的治療途徑,是癲癇治療未來(lái)發(fā)展的方向。近年來(lái)越來(lái)越多的研究表明:癲癇與炎癥密切相關(guān),高遷移率族蛋白1(High mobility group protein 1,HMGB1)是一種重要的細(xì)胞炎癥因子,正常情況下主要存在于細(xì)胞核中,參與維持核小體的結(jié)構(gòu)和基因轉(zhuǎn)錄的調(diào)控,當(dāng)發(fā)生組織損傷時(shí)迅速?gòu)膿p傷的神經(jīng)元、小膠質(zhì)細(xì)胞和星形膠質(zhì)釋放到細(xì)胞外、腦脊液及血清中,它的釋放是觸發(fā)免疫反應(yīng)的危險(xiǎn)信號(hào),在膿毒癥、關(guān)節(jié)炎等多疾病中具有重要的作用,最新研究發(fā)現(xiàn)其與癲癇的發(fā)生也有著緊密的聯(lián)系。Toll樣受體4(Toll-like receptor 4,TLR4)是一種識(shí)別病原相關(guān)分子模式(Pathogen-associated molecular patterns,PAMPs)的受體,能識(shí)別損傷或應(yīng)激所致的“內(nèi)源性危險(xiǎn)信號(hào)”如:HMGB1,激活核轉(zhuǎn)錄因子kappa B(Nuclear factor-k-gene binding,NF-κB)發(fā)生磷酸化,磷酸化的NF-κB(Phosphorylated Nuclear factor-k-gene binding,p-NF-κB)進(jìn)入細(xì)胞核,誘導(dǎo)促炎因子基因表達(dá),腦內(nèi)炎癥導(dǎo)致癲癇反復(fù)發(fā)作。而甘草類藥物有較好的抗炎、抗過(guò)敏和細(xì)胞膜保護(hù)作用,并且有較高的安全性和耐受性,臨床上已廣泛用來(lái)治療肝炎、皮膚病等,最近國(guó)內(nèi)外有研究表明甘草甜素(Glycyrrhizin,GL)作為HMGB1的小分子抑制劑,在炎癥抑制方面有一定作用,并且有較好的安全性和耐受性,且部分藥物可穿過(guò)血腦屏障,有望成為抗癲癇藥物的候選者,但關(guān)于甘草類藥物的神經(jīng)元保護(hù)及抗癲癇作用的機(jī)制,目前還缺乏臨床及實(shí)驗(yàn)數(shù)據(jù)的支持。本研究在用海人酸(Kainic acid,KA)誘導(dǎo)建立幼鼠顳葉癲癇模型的基礎(chǔ)上,采用甘草甜素(Glycyrrhizin,GL)預(yù)處理,通過(guò)觀察行為學(xué)表現(xiàn),探討甘草甜素對(duì)海人酸誘導(dǎo)幼鼠癲癇發(fā)作的敏感性及嚴(yán)重性的影響,利用Western blot與Q-RT-PCR分別從蛋白質(zhì)與mRNA水平檢測(cè)海馬組織HMGB1/TLR4/p-NF-κB的表達(dá),運(yùn)用HE染色及免疫組化從細(xì)胞凋亡水平觀察海馬區(qū)神經(jīng)元的丟失情況,探討甘草甜素可能的抗癲癇及神經(jīng)保護(hù)機(jī)制,及其與腦內(nèi)免疫炎性反應(yīng)的關(guān)系,有望老藥新用,找到癲癇治療的新方向并為其提供理論依據(jù)。材料與方法出生21天的SD大鼠,隨機(jī)分為對(duì)照組、模型Ⅰ組、模型Ⅱ組。模型Ⅰ組用KA誘導(dǎo)癲癇發(fā)作,模型Ⅱ組在應(yīng)用KA前30min腹腔注射GL,模型Ⅰ組根據(jù)觀察時(shí)間點(diǎn)不同分為3h、12h、24h、7d四個(gè)亞組,模型Ⅱ組根據(jù)GL不同劑量分為10mg/kg、50mg/kg、100mg/kg三個(gè)亞組,每個(gè)亞組3只動(dòng)物,行為學(xué)表現(xiàn)按照Racine評(píng)分量表進(jìn)行評(píng)分,RT-PCR檢測(cè)急性期(3h、12h、24h)海馬區(qū)HMGB1/TLR-4 mRNA的表達(dá),Western blot檢測(cè)HMGB1/TLR-4/p-NF-κB蛋白的表達(dá),Elisa檢測(cè)血清中HMGB1蛋白的表達(dá)變化,免疫組化檢測(cè)慢性期(7d)海馬神經(jīng)元抗核抗體(Neu-N)的表達(dá)。結(jié)果1.行為學(xué)結(jié)果:模型Ⅰ組SE發(fā)生率為75%,死亡4只,存活率為:67.3%,SOT:24.08±1.98min;模型Ⅱ組SE發(fā)生率為64.3%,總共死亡6只,存活率85.7%,SOT:33.39±2.66min;生理鹽水對(duì)照組大鼠均未死亡,存活率為100%;GL預(yù)處理模型Ⅱ組與模型Ⅰ組比較,SE發(fā)生率降低,存活率增高,SOT時(shí)間延長(zhǎng)。2.癲癇急性期海馬區(qū)HMGB1/TLR-4基因表達(dá)結(jié)果:模型Ⅰ組與對(duì)照組比較,隨著觀察時(shí)間(3h、12h、24h)的延長(zhǎng),HMGB1、TLR-4基因表達(dá)升高,其中12h時(shí)達(dá)到峰值(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),12h時(shí)間點(diǎn),其中模型Ⅱ組HMGB1、TLR-4基因表達(dá)量較模型Ⅰ組顯著降低(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),不同劑量的干預(yù)的模型Ⅱ組之間無(wú)顯著差異(P0.05)。3.癲癇急性期海馬區(qū)HMGB1/TLR-4/p-NF-κB蛋白表達(dá)結(jié)果:模型Ⅰ組與對(duì)照組比較,隨著觀察時(shí)間(3h、12h、24h)的延長(zhǎng),TLR-4、p-NF-kB蛋白表達(dá)升高,其中12h時(shí)達(dá)到峰值(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),HMGB1的蛋白表達(dá)沒(méi)有明顯變化(P0.05)。在12小時(shí)的時(shí)間點(diǎn),模型Ⅱ組TLR-4、p-NF-k B蛋白表達(dá)量較模型Ⅰ組顯著降低(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),不同劑量的干預(yù)的模型Ⅱ組之間差異不大(P0.05)。4.癲癇急性期血清中HMGB1表達(dá)結(jié)果:模型Ⅰ組與對(duì)照組比較,血清中HMGB1濃度增高,其中12h時(shí)明顯(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),在12h的時(shí)間點(diǎn),模型Ⅱ組與模型Ⅰ組比較,血清中HMGB1的濃度顯著降低(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),不同劑量的干預(yù)的模型Ⅱ組之間差異不大(P0.05)。5.慢性期海馬區(qū)Neu-N表達(dá)結(jié)果:模型Ⅰ組與對(duì)照組比較,海馬區(qū)神經(jīng)元顯著丟失(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),模型Ⅱ組與模型Ⅰ組比較,海馬區(qū)神經(jīng)元的丟失顯著減少(差異具有統(tǒng)計(jì)學(xué)意義,P0.05),不同劑量的干預(yù)的模型Ⅱ組之間差異不大(P0.05)。結(jié)論1.GL預(yù)處理可以延長(zhǎng)幼鼠癲癇發(fā)作的潛伏期,降低癲癇發(fā)作的易感性,減輕幼鼠癲癇的發(fā)作。2.幼鼠癲癇急性期海馬HMGB1/TLR-4基因表達(dá)增加,TLR-4的蛋白表達(dá)增高,誘導(dǎo)NF-κB的磷酸化。3.GL預(yù)處理可以降低HMGB1的基因合成及釋放,降低胞外HMGB1濃度,降低TLR-4的基因表達(dá)及蛋白合成,抑制NF-κB的磷酸化。4.GL預(yù)處理能減輕癲癇所致的海馬區(qū)病理性損害,預(yù)防神經(jīng)元的丟失,發(fā)揮一定的神經(jīng)保護(hù)作用。
[Abstract]:Background and objective epilepsy is a common chronic nervous system disease in childhood. Epilepsy patients in 70-80% can control epileptic seizures by antiepileptic drugs, but there are still about 20-30% of epileptic patients who still have seizures after receiving standardized and reasonable antiepileptic drugs. Temporal lobe epilepsy is difficult to treat epilepsy. A large number of studies have shown that recurrent seizures of temporal lobe epilepsy can cause loss of neurons in the hippocampus and hippocampus sclerosis, which not only affects the life and work of the patients, but also causes a great burden on the family and society. The current antiepileptic drugs are mainly responsible for the effect of antiepileptic drugs. The ion channel, which inhibits the excitatory of neurons, carries out symptomatic treatment, studies the etiology and pathogenesis of epilepsy, finds new drugs and seeks new ways of treatment in the key link of the seizure mechanism. It is the direction of the future development of epilepsy treatment. In recent years, more and more studies have shown that epilepsy is closely related to inflammation and high mobility group. Protein 1 (High mobility group protein 1, HMGB1) is an important cell inflammatory factor, which is normally present in the nucleus and is involved in the maintenance of the structure of the nucleosome and the regulation of gene transcription. When tissue damage occurs, it is quickly released from the damaged neurons, microglia and astrocytes to the extracellular, cerebrospinal fluid and serum. Its release is a dangerous signal to trigger the immune response and plays an important role in many diseases such as sepsis and arthritis. The latest research has found that it is closely related to the occurrence of epilepsy..Toll like receptor 4 (Toll-like receptor 4, TLR4) is a type of Pathogen-associated molecular patterns, PAM (PAM). Ps) receptors can identify "endogenous risk signals" caused by injury or stress, such as HMGB1, the activation of the nuclear transcription factor kappa B (Nuclear factor-k-gene binding, NF- kappa B), and the phosphorylation of NF- kappa B into the nucleus, inducing the gene expression of proinflammatory factors, and inflammation in the brain. It causes recurrent seizures, and Glycyrrhiza drugs have good anti-inflammatory, anti allergy and cell membrane protection, and have high safety and tolerance. It has been widely used in the treatment of hepatitis, dermatosis and so on. Recently, studies have shown that Glycyrrhizin (GL) is a small molecule inhibitor of HMGB1, in the area of inflammation inhibition. There is a certain effect, good safety and tolerance, and some drugs can pass through the blood brain barrier, which is expected to be a candidate for antiepileptic drugs. However, the mechanism of the protective and antiepileptic effects of Glycyrrhiza drugs is still lacking the support of clinical and experimental data. This study was induced by Kainic acid (KA). On the basis of the model of temporal lobe epilepsy in young rats, the effects of glycyrrhizin on the susceptibility and severity of epileptic seizures in young rats induced by glycyrrhizin were investigated by Glycyrrhizin (GL) preconditioning, and HMGB1/TLR4/p-NF- kappa B in hippocampus was detected from protein and mRNA levels by Western blot and Q-RT-PCR. Using HE staining and immunohistochemistry to observe the loss of neurons in the hippocampus from the level of apoptosis, explore the possible antiepileptic and neuroprotective mechanisms of glycyrrhizin, and its relationship with the immunological reaction in the brain. It is hopeful that the old drug can be used to find new directions for the treatment of epilepsy and provide a theoretical basis for it. Materials and methods are born. 21 days of SD rats were randomly divided into control group, model I group, model II group. Model I group used KA to induce epileptic seizures. Group II group was injected GL before KA 30min, model I group was divided into 3h, 12h, 24h, 7d subgroups according to the observation time points, and the model II group was divided into 10mg/kg, 50mg/kg, and three subgroups according to GL different doses, each group. In the subgroup, 3 animals were scored according to the Racine scale. RT-PCR was used to detect the expression of HMGB1/TLR-4 mRNA in the hippocampus of the acute phase (3H, 12h, 24h), the expression of HMGB1/TLR-4/p-NF- kappa B protein in Western blot, the expression of the protein in the Elisa test serum, and the immunohistochemical detection of the anti nuclear antibody of the hippocampal neurons in the chronic period. Results 1. the results of 1. behavior: the incidence of SE in model I group was 75%, and 4 died, the survival rate was 67.3%, SOT:24.08 + 1.98min; the incidence of SE in the model II group was 64.3%, the total mortality was 6, the survival rate was 85.7%, SOT:33.39 + 2.66min; the normal saline control group was not dead and the survival rate was 100%; GL Preconditioning Model II group and model I group were compared. In comparison, the incidence of SE decreased, the survival rate increased, and the SOT time prolonged the expression of HMGB1/TLR-4 gene in the hippocampus of.2.: model I was compared with the control group. With the prolongation of the observation time (3H, 12h, 24h), the expression of HMGB1 and TLR-4 increased, in which 12h reached the peak value (the difference was statistically significant, P0.05), and the 12h time point, model II Group HMGB1, TLR-4 gene expression was significantly lower than that in model I group (the difference was statistically significant, P0.05). There was no significant difference between the model II groups with different doses of intervention (P0.05) the expression of HMGB1/TLR-4/p-NF- kappa B protein in the hippocampus of.3. epileptic period of.3.: the model I group was compared with the control group, with the prolongation of the observation time (3H, 12h, 24h), TLR-4, The expression of p-NF-kB protein increased, of which 12h reached its peak value (the difference was statistically significant, P0.05), and there was no significant change in the protein expression of HMGB1 (P0.05). In the 12 hour time point, the expression of p-NF-k B protein in model II group was significantly lower than that in the model I group (the difference was statistically significant, P0.05), and the model II Group intervened in different doses. The results of HMGB1 expression in serum of P0.05.4. epileptic acute phase: in model I group, the concentration of HMGB1 in serum was higher than that in control group, of which 12h was significant (the difference was statistically significant, P0.05). In the time point of 12h, the concentration of HMGB1 in the model II Group was significantly reduced (the difference was statistically significant, P0., P0., P0.). 05), there was no significant difference between the model II groups in different doses of intervention (P0.05).5. chronic hippocampal Neu-N expression results: compared with the control group, the hippocampal neurons were significantly lost in model I group (the difference was statistically significant, P0.05). The loss of neurons in the hippocampus was significantly reduced in model II group and model I group (the difference was statistically significant. P0.05), there was little difference between the model II groups with different doses of intervention (P0.05). Conclusion 1.GL pretreatment could prolong the incubation period of epileptic seizures in young rats, reduce the susceptibility of epileptic seizures, reduce the expression of HMGB1/TLR-4 gene expression in hippocampus of young rats with epileptic seizures, increase the expression of TLR-4 protein and induce the phosphorus of NF- kappa B. Acidified.3.GL pretreatment can reduce the gene synthesis and release of HMGB1, reduce the concentration of extracellular HMGB1, reduce the gene expression and protein synthesis of TLR-4, and inhibit the phosphorylated.4.GL pretreatment of NF- kappa B to reduce the pathological damage in the hippocampus, prevent the loss of neurons and play a certain neuroprotective effect.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R742.1

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