【摘要】：目的觀察偏釩酸鈉亞慢性經(jīng)口染毒所致大鼠學(xué)習(xí)記憶損傷情況,探討其對(duì)紋狀體神經(jīng)細(xì)胞凋亡的影響。方法無特定病原體級(jí)健康雄性SD大鼠32只,隨機(jī)分為對(duì)照組及低、中、高劑量組,每組8只。分別予質(zhì)量濃度為0.0、0.5、1.0、2.0 g/L偏釩酸鈉水溶液經(jīng)口飲水染毒3個(gè)月后,采用Morris水迷宮實(shí)驗(yàn)測(cè)試大鼠學(xué)習(xí)記憶能力,分離大鼠紋狀體觀察神經(jīng)細(xì)胞形態(tài)學(xué)改變并以流式細(xì)胞儀檢測(cè)其神經(jīng)細(xì)胞凋亡率。結(jié)果對(duì)照組和低、中、高劑量組大鼠平均逃避潛伏期分別為(37.43±8.82)、(45.71±12.44)、(59.74±22.91)、(68.45±12.06)s;中劑量組大鼠逃避潛伏期高于對(duì)照組(P0.05),高劑量組大鼠逃避潛伏期分別高于對(duì)照組和低劑量組(P0.05)。4組大鼠穿越平臺(tái)次數(shù)中位數(shù)(M)分別為3.5、3.0、2.0和2.0次;中和高劑量組穿越平臺(tái)次數(shù)均低于對(duì)照組(P0.05)。4組大鼠腦紋狀體神經(jīng)細(xì)胞早期凋亡率M分別為2.15%、5.45%、9.50%和13.55%,晚期凋亡率M分別為0.05%、0.15%、0.35%和0.75%,總凋亡率M分別為2.35%、5.60%、9.80%和14.65%;中和高劑量組紋狀體神經(jīng)細(xì)胞早期凋亡率、總凋亡率均分別高于對(duì)照組(P0.05)。病理組織學(xué)檢查結(jié)果顯示:大鼠紋狀體組織疏松、水腫、空泡變性,可見細(xì)胞凋亡形態(tài)。Spearman相關(guān)分析顯示:釩染毒大鼠的逃避潛伏期與紋狀體神經(jīng)細(xì)胞早期凋亡率和總凋亡率均呈正相關(guān)[Spearman相關(guān)系數(shù)(rS)分別為0.615和0.565,P0.05];穿越平臺(tái)次數(shù)與紋狀體神經(jīng)細(xì)胞早期凋亡率和總凋亡率均呈負(fù)相關(guān)(rS分別為-0.450和-0.483,P0.05)。結(jié)論偏釩酸鈉可通過介導(dǎo)紋狀體神經(jīng)細(xì)胞凋亡增加而損傷大鼠學(xué)習(xí)記憶能力。
[Abstract]:Objective to observe the learning and memory impairment induced by sodium metavanadate subchronic oral exposure in rats and to explore the effect of sodium metavanadate on neuronal apoptosis in striatum. Methods 32 healthy male SD rats without specific pathogen grade were randomly divided into control group (n = 8) and low, middle and high dose group (n = 8). The learning and memory ability of rats was tested by Morris water maze test after exposure to sodium metavanadate aqueous solution of 0.0,0.5, 1.0g and 2.0g 脳 L sodium metavanadate solution through oral drinking water for 3 months. The morphological changes of nerve cells were observed in striatum of rats and the apoptosis rate of nerve cells was detected by flow cytometry. Results the average escape latency of control group and low, middle and high dose group was (37.43 鹵8.82), (45.71 鹵12.44), (59.74 鹵22.91), (68.45 鹵12.06) s, respectively. The escape latency in the middle dose group was higher than that in the control group (P 0.05). The escape latency in the high dose group was higher than that in the control group and the low dose group (P 0.05). The median (M) of the number of crossing the platform in the 4 groups was 3.5, 3.0, 2.0 and 2.0 times, respectively. The number of crossing the platform in the middle and high dose groups was lower than that in the control group (P 0.05). The early apoptosis rate M of striatum neurons in 4 groups was 2.15%, 5.45%, 9.50% and 13.55%, respectively. The late apoptosis rate M was 0.05%, 0.15%, 0.35% and 0.75%, respectively. The total apoptosis rate M was 2.35%, 5.60%, 9.80% and 14.65%, respectively. The early apoptosis rate and total apoptosis rate of striatum neurons in middle and high dose groups were higher than those in control group (P 0.05). The results of pathological histology showed that the striatum of rats was loose, edema and vacuole degeneration. Spearman correlation analysis showed that the escape latency of vanadium exposed rats was positively correlated with the early apoptosis rate and total apoptosis rate of striatal nerve cells [Spearman correlation coefficient (rS) was 0.615 and 0.565, respectively, P 0.05]. The number of crossing the platform was negatively correlated with the early apoptosis rate and the total apoptosis rate of striatal nerve cells (rS =-0.450 and-0.483, respectively, P 0.05). Conclusion Sodium metavadate can damage the learning and memory ability of rats by mediating the increase of neuronal apoptosis in striatum.
【作者單位】： 遵義醫(yī)學(xué)院公共衛(wèi)生學(xué)院
【基金】：貴州省聯(lián)合基金(CK-1002)
【分類號(hào)】：R114

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