本文選題：高脂血癥 + 腦缺血��； 參考：《北京中醫(yī)藥大學(xué)》2012年博士論文

【摘要】：1.背景 單純腦缺血在臨床上發(fā)病率較低,僅見(jiàn)于房顫附壁血栓脫落、感染性膿栓、脂肪性栓子、癌細(xì)胞栓子、寄生蟲(chóng)卵栓子等引起的栓塞。大多數(shù)腦缺血是在某些基礎(chǔ)病變條件下發(fā)生的,如高血壓、高脂血癥、糖尿病等；這些基礎(chǔ)性病變本身就是缺血性中風(fēng)的高危因素,在其影響或作用下,腦缺血性雖然伴隨腦水腫、血液高凝狀態(tài)、自由基損傷、炎癥反應(yīng)、神經(jīng)細(xì)胞壞死及凋亡等共同的病理生理過(guò)程,但是也存在一些差異,如缺血程度、炎癥反應(yīng)、神經(jīng)功能缺損的程度及神經(jīng)細(xì)胞死亡的方式等并不完全一樣。這些差異可能在整個(gè)病理過(guò)程中起重要作用；而采用同一的治療方案很難達(dá)到滿意的治療效果。目前,已經(jīng)上市的治療中風(fēng)的新藥很少是針對(duì)帶有某種基礎(chǔ)性病變而研發(fā)的。 中醫(yī)對(duì)缺血性中風(fēng)有著豐富的認(rèn)識(shí),其病因主要涉及“風(fēng)、火、痰、瘀、虛”；病因不同,中風(fēng)后表現(xiàn)亦有區(qū)別；針對(duì)不同證型,采用對(duì)癥的方藥進(jìn)行治療,療效顯著；中醫(yī)對(duì)中風(fēng)的辯證施治,體現(xiàn)了中醫(yī)在治療復(fù)雜疾病中的優(yōu)勢(shì)。 本研究擬把中醫(yī)病機(jī)理論與現(xiàn)代醫(yī)學(xué)病理、病理生理理論系統(tǒng)結(jié)合起來(lái),針對(duì)在某些基礎(chǔ)病變(證型)條件下構(gòu)建腦缺血復(fù)合模型,相對(duì)接近臨床實(shí)際,為探討中藥復(fù)方的藥理機(jī)制和對(duì)證治療療效評(píng)價(jià)提供規(guī)范的模型基礎(chǔ)。 2.目的 1)研究高脂血癥大鼠模型炎癥反應(yīng)狀態(tài)及腦組織的影響,比較高脂血癥大鼠模型和正常大鼠腦組織的病理性差異,分析高脂血癥大鼠模型腦組織的病理學(xué)特點(diǎn)。 2)比較復(fù)合腦缺血模型和單純腦缺血模型在不同時(shí)間炎癥反應(yīng)變化及對(duì)神經(jīng)-血管單元的影響,研究在高脂血癥條件下腦缺血病變的特異性變化,分析高脂血癥炎癥因素對(duì)缺血腦組織的影響。 3.方法 1)造模：采用高脂飼料飼養(yǎng)大鼠,復(fù)制經(jīng)典的高脂血癥動(dòng)物模型,檢測(cè)大鼠血清中血脂的含量以確定模型成功；復(fù)制大腦中動(dòng)脈缺血模型,觀察大鼠腦部缺血損傷情況。 2)分組：將實(shí)驗(yàn)大鼠分為正常組、假手術(shù)組、單純腦缺血3d組、單純腦缺血7d組與高脂血癥組、高脂血癥假手術(shù)組、復(fù)合腦缺血3d組、復(fù)合腦缺血7d組,采用神經(jīng)功能評(píng)分和TTC染色的方法,檢測(cè)不同組間動(dòng)物的行為功能,并觀察腦組織梗死體積。 3)斷尾取血,酶聯(lián)免疫法(ELISA)檢測(cè)血清中ET-1、NO、6-keto-FGF1a、TX-B2、MCP-1、TNF-α、CRP、SOD、MDA和vWF含量。 4)免疫組織化學(xué)方法比較各組大鼠腦組織MMP-2、ICAM-1、Bax、Bcl-2和CD34表達(dá)。 5)HE染色的方法觀察各組大鼠腦組織梗死邊緣區(qū)組織病理學(xué)改變。 6)利用透射電鏡技術(shù),觀察各組大鼠腦組織梗死邊緣區(qū)細(xì)胞超微結(jié)構(gòu)改變。 4.結(jié)果 1)高脂血癥組與正常組比較 ①高脂血癥組血清中NO、6-keto-FGF1a含量減少,差異顯著(0.01p0.05)；TX-B2含量增多,差異顯著(p0.05)；MCP-1、TNF-α、CRP、vWF、MDA含量明顯增多,差異顯著(p0.01)；腦組織中MMP-2、ICAM-1和CD34的表達(dá)增高,差異顯著性(0.01P0.05)。 ②高脂血癥組神經(jīng)元有少量萎縮,線粒體嵴變短,粗面內(nèi)質(zhì)網(wǎng)減少；皮質(zhì)區(qū)毛細(xì)血管增多,血管內(nèi)皮細(xì)胞線粒體及線粒體嵴增多；神經(jīng)膠質(zhì)細(xì)胞增多明顯,線粒體嵴豐富；神經(jīng)突觸地突觸小泡減少,線粒體嵴變短。 2)復(fù)合腦缺血組與單純腦缺血組相比較： ①兩模型組在缺血3d、7d神經(jīng)功能評(píng)分無(wú)差異,但造模大鼠蘇醒后和缺血3d、7d神經(jīng)功能評(píng)分的差值比較,復(fù)合腦缺血組缺血7d差值減小,差異顯著(p0.05)。 ②復(fù)合腦缺血組缺血7d梗死體積縮小,差異顯著(p0.05),缺血3d無(wú)差異(P0.05)。 ③NO、6-keto-FGF1a在復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,腦缺血組在缺血3d、7d血清含量均高于相應(yīng)的假手術(shù)組,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組在缺血3d、7d血清含量均減少,但在缺血3d組間比較無(wú)明顯差異(P0.05),缺血7d組間比較差異顯著(p0.05)。 ④ET-1在腦缺血模型各時(shí)間點(diǎn)血清含量呈增多趨勢(shì),但復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)及組間比較無(wú)顯著性差異(P0.05)。TX-B2在腦缺血模型各時(shí)間點(diǎn)血清含量呈增多趨勢(shì),單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,在缺血3d、7d血清含量增多,差異顯著(p0.05),復(fù)合腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,在缺血3d、7d血清含量呈增多趨勢(shì),但差異無(wú)顯著性(P0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組血清含量減少,缺血3d、7d差異均顯著(p0.05)。 ⑤vWF因子在腦缺血模型各時(shí)間點(diǎn)血清含量呈增多趨勢(shì),單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,單純腦缺血組再缺血7d血清含量增多,差異顯著(p0.05)；復(fù)合腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,復(fù)合腦缺血組在缺血3 d血清含量增多,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組在缺血3d、7d血清含量均增多,差異顯著(p0.05)。 ⑥MCP-1、TNF-α和CRP在復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,腦缺血組在缺血3d、7d血清含量均多于相應(yīng)的假手術(shù)組,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組在缺血3d、7d血清含量均增多,差異顯著(p0.05,0.01p0.05)。 ⑦M(jìn)MP-2、ICAM-1、CD34在復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,腦缺血組在缺血3d、7d腦組織的表達(dá)均高于相應(yīng)的假手術(shù)組,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組缺血3d、7d腦組織中表達(dá)均增高,差異顯著(p0.05,0.01P0.05)。 ⑧MDA在單純腦缺血組與假手術(shù)組組內(nèi)比較,缺血3d血清中含量增多,差異顯著(p0.05)；復(fù)合腦缺血組與高脂血癥假手術(shù)組組內(nèi)比較,缺血3d、7d血清中含量均減少,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組在缺血3d、7d血清中含量均減少,差異顯著(p0.05)。SOD在復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,腦缺血組在缺血3d、7d血清含量均減少,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,復(fù)合腦缺血組在缺血3d血清含量減少,差異顯著(p0.05)。 ⑨Bcl-2、Bax在復(fù)合腦缺血組和單純腦缺血組與相應(yīng)假手術(shù)組組內(nèi)比較,腦缺血組在缺血3d、7d在腦組織中的表達(dá)均增高,差異顯著(p0.05)；復(fù)合腦缺血組與單純腦缺血組組間比較,Bax在復(fù)合腦缺血組腦組織中表達(dá)3d、7d均下降,差異顯著(p0.05)；Bcl-2在缺血3d表達(dá)增高,差異顯著(p0.05)；Bcl-2/Bax比值在復(fù)合腦缺血組3d、7d均升高,差異顯著(p0.05)。 ⑩缺血邊緣組織學(xué)觀察,復(fù)合腦缺血組與單純腦缺血組比較,缺血3d均有大量神經(jīng)元變性、壞死,核染色質(zhì)稀疏,線粒體嵴變短或消失、嵴間腔擴(kuò)大,粗面內(nèi)質(zhì)網(wǎng)明顯減少；血管內(nèi)皮細(xì)胞腫脹,細(xì)胞連接破壞,線粒體及線粒體嵴減少；神經(jīng)膠質(zhì)細(xì)胞反應(yīng)增生明顯,線粒體嵴變短或消失；有小膠質(zhì)細(xì)胞增生；神經(jīng)突觸地突觸小泡減少,線粒體嵴變短或消失。缺血7d上述損傷減輕,復(fù)合腦缺血組與單純腦缺血組比較神經(jīng)元變性、壞死減少,水腫減輕,線粒體損傷恢復(fù)；神經(jīng)膠質(zhì)細(xì)胞增多明顯,線粒體嵴豐富；內(nèi)皮細(xì)胞水腫減輕。 5.結(jié)論 1)高脂血癥病變過(guò)程中,病變損傷血管內(nèi)皮細(xì)胞,誘發(fā)腦組織的炎癥反應(yīng),并對(duì)血管-神經(jīng)元產(chǎn)生一定的影響； 2)炎癥及炎癥相關(guān)因子可能是痰濕、瘀血中醫(yī)病機(jī)的部分生物學(xué)基礎(chǔ)； 3)高脂血癥條件下,炎癥因子在缺血不同時(shí)期既有累積現(xiàn)象,又有特異性的表達(dá),這可能在腦缺血恢復(fù)期有助于損傷的修復(fù)； 4)在炎癥反應(yīng)提前預(yù)刺激下,內(nèi)源性的腦保護(hù)機(jī)制可能被啟動(dòng)。
[Abstract]:1. background
The incidence of simple cerebral ischemia is low in clinical, only in the embolus caused by atrial fibrillation, septic suppository, fatty embolus, cancer cell embolus, and parasitic oocyte embolus. Most cerebral ischemia occurs under certain basic pathological conditions, such as hypertension, hyperlipidemia, diabetes and so on; these basic lesions themselves are The high risk factors of ischemic apoplexy, in which the ischemic stroke is associated with brain edema, hypercoagulability, free radical damage, inflammation, necrosis of the nerve cells and apoptosis, but there are also some differences, such as the degree of ischemia, the inflammation, the degree of nerve function defect and the death of the nerve cells. The ways of dying are not exactly the same. These differences may play an important role in the whole pathological process; and the same treatment is difficult to achieve satisfactory results.
Chinese medicine has a rich understanding of ischemic stroke, its cause is mainly involved in "wind, fire, phlegm, stasis, deficiency"; the cause is different and the performance is different after the stroke; the curative effect is remarkable for the different syndromes, using the prescriptions of the symptomatic, the dialectical treatment of stroke, embodies the advantages of traditional Chinese medicine in the treatment of complex diseases.
This study is to combine the theory of pathogenesis of traditional Chinese medicine with the modern medical pathology and pathophysiology system, and to construct a complex model of cerebral ischemia under certain basic pathological conditions (syndrome type), which is relatively close to the clinical practice, and provides a standard model basis for the study of the pharmacological mechanism of Chinese medicine compound and the evaluation of the therapeutic effect of the syndrome treatment.
2. purposes
1) to study the effect of inflammatory reaction and brain tissue in hyperlipidemia rat model, compare the pathological difference between hyperlipidemia rat model and normal rat brain tissue, and analyze the pathological characteristics of brain tissue of hyperlipidemia rat model.
2) to compare the changes of the inflammatory response and the effects on the neurovascular units of the complex cerebral ischemia model and the simple cerebral ischemia model at different time and to study the specific changes of the cerebral ischemia in the hyperlipidemia condition, and to analyze the effect of the inflammatory factors of hyperlipidemia to the ischemic brain tissue.
3. method
1) model: feeding rats with high fat feed, replicating the classic hyperlipidemia animal model, detecting the serum lipid content in rats to determine the model success, replicating the cerebral ischemia model of the middle cerebral artery, and observing the cerebral ischemia injury in the rat.
2) group: the experimental rats were divided into normal group, sham operation group, simple cerebral ischemia 3D group, simple cerebral ischemia 7d group and hyperlipidemia group, hyperlipidemia sham group, compound cerebral ischemia 3D group, complex cerebral ischemia 7d group, neural function score and TTC staining method, the behavioral function of different groups were detected and the infarct volume of brain tissue was observed.
3) blood samples were taken from the tail, and the levels of ET-1, NO, 6-keto-FGF1a, TX-B2, MCP-1, TNF-, CRP, SOD, MDA and vWF in serum were detected by enzyme linked immunosorbent assay (ELISA).
4) immunohistochemical method was used to compare the expression of MMP-2, ICAM-1, Bax, Bcl-2 and CD34 in brain tissue of each group.
5) HE staining method was used to observe the histopathological changes in the marginal area of cerebral infarction in each group.
6) transmission electron microscopy was used to observe the ultrastructural changes in the marginal area of infarct of rats in each group.
4. results
1) comparison of hyperlipidemia group and normal group
(1) the levels of NO and 6-keto-FGF1a in the serum of hyperlipidemia group were decreased (0.01p0.05), and the content of TX-B2 increased significantly (P0.05); MCP-1, TNF- a, CRP, vWF and MDA increased significantly (P0.01).
2. The neurons in the hyperlipidemia group had a small amount of atrophy, the mitochondrial crista shortened, the rough endoplasmic reticulum decreased, the capillary vessels in the cortex increased, the mitochondria and mitochondrial crista of the vascular endothelial cells increased, the glial cells increased obviously, the mitochondrial crista was rich, the synapse vesicles decreased and the mitochondrial crista became shorter.
2) the compound cerebral ischemia group was compared with the simple cerebral ischemia group.
(1) there was no difference between the two model group in the ischemic 3D and the 7d nerve function score, but the difference between the model rats after awakening and the ischemic 3D, and the difference of the 7d nerve function score, the difference of the 7d difference between the compound cerebral ischemia group and the ischemic group was significantly decreased (P0.05).
(2) the infarct volume of 7D in the combined cerebral ischemia group was significantly reduced (P0.05), and there was no difference in ischemic 3D (P0.05).
(3) NO, 6-keto-FGF1a was compared in the complex cerebral ischemia group and the simple cerebral ischemia group and the corresponding sham operation group. The serum content of 3D in the ischemic group was higher than that in the corresponding sham operation group, and the difference was significant (P0.05). The ischemic group and the simple cerebral ischemia group were compared with the ischemic group in the ischemic group, and the serum content of 7D decreased in the ischemic 3D and 7d in the ischemic group, but in the ischemic group, the serum content of 7D was decreased, but in the ischemic group, the serum content of 7D was reduced. There was no significant difference in ischemic 3D between groups (P0.05), but there was a significant difference between ischemic 7d groups (P0.05).
(4) the serum content of ET-1 was increased in each time point of cerebral ischemia model, but there was no significant difference between the combined cerebral ischemia group and the group of simple cerebral ischemia and the corresponding sham operation group (P0.05). The serum content of.TX-B2 in the cerebral ischemia model increased, and the ischemia group and the corresponding sham operation group were compared with the corresponding sham operation group, and in the ischemia group, the.TX-B2 was in ischemia. The serum content of 3D and 7d increased significantly (P0.05). Compared with the corresponding sham operation group, the serum content of 7D in the ischemic group and the corresponding sham operation group was increased, but there was no significant difference (P0.05) in the ischemic 3D, but in the compound cerebral ischemia group and the simple cerebral ischemia group, the serum content of the complex cerebral ischemia group decreased, and the difference of 3D and 7d in ischemia was significant (P0.05).
(5) the serum content of vWF factor increased in the cerebral ischemia model at all time points. Compared with the corresponding sham operation group, the serum content of 7D increased significantly in the simple cerebral ischemia group, and the difference was significant (P0.05). In the compound cerebral ischemia group and the corresponding sham operation group, the serum content of 3 D in the complex cerebral ischemia group increased, and the difference between the cerebral ischemia group and the corresponding sham operation group increased. Significant (P0.05); compared with the simple cerebral ischemia group, the serum levels of 3D and 7d in the combined cerebral ischemia group increased significantly (P0.05).
(6) MCP-1, TNF- alpha and CRP were compared in the complex cerebral ischemia group and the simple cerebral ischemia group and the corresponding sham operation group. The serum content of the ischemic group was more than that of the corresponding sham operation group, and the serum content of 7D was significantly higher than that of the corresponding sham operation group (P0.05). The complex cerebral ischemia group was compared with the simple cerebral ischemia group, and the serum content of the ischemic group was increased in the ischemic group of 3D, and the serum level of 7D was more than that of the group of cerebral ischemia. The serum content of 7D in the complex cerebral ischemia group increased and the serum level of 7D was increased. Different significance (p0.05,0.01p0.05).
MMP-2, ICAM-1, CD34 were compared in the group of ischemic cerebral ischemia and simple cerebral ischemia group and the corresponding sham operation group. The expression of 3D in ischemic group was higher than that in the corresponding sham operation group, and the difference was significant (P0.05). The expression of 3D in the compound cerebral ischemia group was more than that in the ischemic group, and the expression of 3D in the complex cerebral ischemia group was increased and the expression of 7D brain tissue increased. The difference was significant (p0.05,0.01P0.05).
Compared with the group of pure cerebral ischemia and sham operation group, the content of ischemic 3D in the serum was increased, the difference was significant (P0.05), and the content of ischemic 3D and 7d in the compound cerebral ischemia group and the hyperlipidemic sham group were decreased, the difference was significant (P0.05), and the complex cerebral ischemia group was less than the group of simple cerebral ischemia group, and the complex cerebral ischemia group was deficient in the group of cerebral ischemia. The blood 3D, 7d serum content decreased significantly (P0.05).SOD in the complex cerebral ischemia group and the Dan Chunnao ischemia group and the corresponding sham group, the cerebral ischemia group was in the ischemic 3D, 7d serum content decreased, the difference was significant (P0.05), the compound cerebral ischemia group was compared with the simple cerebral ischemia group, the complex cerebral ischemia group decreased the serum level of ischemic 3D in the ischemic group. The difference was significant (P0.05).
Bcl-2, Bax in cerebral ischemia group and simple cerebral ischemia group and the corresponding sham operation group, cerebral ischemia group in ischemic 3D, 7d expression in the brain tissue increased, the difference was significant (P0.05), Bax in the cerebral ischemia group compared with the simple cerebral ischemia group, Bax in the brain tissue of the complex brain tissue expression 3D, 7d decreased significantly (P0.05). The expression of Bcl-2 in ischemic 3D increased significantly (P0.05), and Bcl-2/Bax ratio increased significantly in 3D group and 7d group (P0.05).
Compared with the simple cerebral ischemia group, the ischemic 3D had a large number of neurons denatured, necrotic, the nucleus chromatin was sparse, the mitochondrial crista shortened or disappeared, the intercristal cavity enlarged and the rough endoplasmic reticulum decreased obviously; the vascular endothelial cells were swollen, the cell connection was destroyed, the mitochondria and mitochondrial crista were reduced; nerve gum was reduced. The mitochondrial crista became short or disappearing in the mitochondrial crista; there were microgliosis, the synaptic vesicles decreased, the mitochondrial crista shortened or disappeared. The ischemic 7d was reduced, and the complex cerebral ischemia group compared with the simple cerebral ischemia group, the neuron degeneration, the decrease of necrosis, the decrease of edema, the recovery of mitochondrial damage and the glia. The number of cells increased obviously, the mitochondria cristae were abundant, and the edema of endothelial cells was alleviated.
5. conclusion
1) during hyperlipidemia, lesions can damage vascular endothelial cells, induce inflammatory reaction in the brain tissue, and have a certain effect on blood vessels and neurons.
2) inflammation and inflammation related factors may be part of the biological basis of TCM pathogenesis of phlegm dampness and blood stasis.
3) under the condition of hyperlipidemia, the inflammatory factors have both accumulation and specific expression in different periods of ischemia, which may contribute to the repair of injury in the recovery period of cerebral ischemia.
4) the endogenous brain protection mechanism may be activated under the pre stimulation of inflammation.
【學(xué)位授予單位】：北京中醫(yī)藥大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類號(hào)】：R589.2;R-332

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