顳葉癲癇病人海馬迴中熱休克蛋白和細胞凋亡的表現; Expressions of heat shock proteins and apoptosis in the hippocampus in human temporal lobe epilepsy

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Title:	顳葉癲癇病人海馬迴中熱休克蛋白和細胞凋亡的表現;Expressions of heat shock proteins and apoptosis in the hippocampus in human temporal lobe epilepsy
Authors:	周逸華;I-Hua Chou
Contributors:	中國醫藥學院醫學研究所
Keywords:	顳葉癲癇;熱休克蛋白;細胞凋亡;temporal lobe epilepsy;heat shock proteins;apoptosis
Date:	1990
Issue Date:	2009-12-03 09:26:30 (UTC+8)
Abstract:	顳葉癲癇 ( TLE ) 為複雜性局部發作，當癲癇患者以藥物治療效果不彰或有副作用產生時，可考慮施以顳葉切除術將電位發作病灶切除或隔離。當細胞曝露在stress之下，會誘導熱休克蛋白 ( HSPs ) 的表現，此引發型的HSPs具有保護細胞的功能。近年，在kainic acid誘導癲癇發作的動物模式研究中，發現HSP70和HSP27在海馬迴的表現會增加。可是在TLE病人大腦組織的HSP70和HSP27表現如何尚未有研究報告，而病理表現出神經細胞減少的現象，其發生的原因亦不是完全明瞭。本研究收集顳葉切除的TLE病人之大腦組織，包括顳葉和海馬迴兩部份，發作部位皆在海馬迴，而顳葉部份並無不正常之放電情形出現。在海馬迴可觀察到神經細胞減少、神經膠細胞增生和海馬迴硬化現象出現，顳葉部份則無此現象。利用TUNEL方法，偵測細胞凋亡在海馬迴組織有明顯增加現象。另外以免疫組織化學染色法來分析凋亡促進蛋白Bax和HSP70、HSP27的表現情形，結果顯示在TLE病人的海馬迴組織中，HSP70和HSP27主要被誘導表現在神經膠細胞，並觀察到Bax的表現呈現增加的情形，與顳葉組織相比，具有統計上的差異。由實驗結果可推論：細胞凋亡作用是造成TLE病人的海馬迴組織中細胞減少的原因之一，在海馬迴組織中表現增加的Bax蛋白質，則可促使此凋亡作用的進行。發作部位之海馬迴在受到stress之狀況下，可被誘導表現出HSP70和HSP27以保護細胞，HSP70和HSP27主要表現在神經膠細胞，可推測膠細胞對stress是較其他神經細胞更有抵抗性。; Heat shock proteins (HSPs) are induced by a variety of insults in the nervous system. We investigated the expression of HSP70, HSP27 and the apoptosis-associated Bax protein in hippocampal subfields of lobectomy specimens from temporal lobe epilepsy (TLE) patients. The pathologic findings showed severe hippocampal neuron losses and gliosis in surgical specimens. The mean percentage of apoptotic cells detected by TUNEL method in the hippocampus was 9.02% and that in the temporal lobe was 2.24%. It was statistically higher of apoptotic cells in the hippocampus compared with the temporal lobe in TLE (P<0.005). The increased expression of apoptosis-promoting Bax protein was observed in the hippocampus in all cases of TLE, whereas, there were weak and few signals in the temporal lobe in TLE and non-epileptic control autopsied tissue. Increased immunoreactivities for HSP70 and HSP27 were observed in glial cells in the hippocampus in TLE. HSP70 was detectable in 7.54% of glial cells in the hippocampus and HSP27 was 3.29%. The percentages of HSP70 and HSP27-positive cells were statistically higher in the hippocampus than in the temporal lobe (P<0.005 and P<0.05). We interpret these interesting findings as evidence of a possible apoptotic mechanism, which lead to hippocampal cell death in TLE. The expressions of HSP70 and HSP27 in glial cells in the hippocampus suggest that they might play some role in remolding the injured region of the CNS.
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