Abstract：
Objective: To explore the effect of the absent in melanoma 2 (AIM2) -mediated neuroinflammation in noise-induced cognitive dysfunction in rats. Methods: In April 2023, sixteen male Wistar rats were randomly divided into control group and noise group, with 8 rats in each group. The rats in the noise group were placed in 50 cm×50 cm×40 cm transparent boxes and exposed to 100 dB (A) white noise with a sound pressure level of 100 dB (A) (4 h/d for 30 d) . At the same time, rats in the control group were kept in similar boxes with environmental noise less than 60 dB (A) . After 30 days of noise exposure, the Morris water maze experiment was applied to test the learning and memory abilities of the rats; the pathological morphology of hippocampal tissues was observed by Hematoxylin-Eosin (HE) staining. Western blot was used to detect the protein expression levels of AIM2, cysteinyl aspartate specific proteinase-1 (caspase-1) , apoptosis-associated speck-like protein (ASC) , interleukin-1β (IL-1β) , IL-18, ionic calcium-binding articulation molecule-1 (Iba-1) , and glial fibrillary acidic protein (GFAP) . The expression of both Iba-1 and GFAP in hippocampal tissue was assessed by immunohistochemical staining. The co-localization of AIM2 with Iba-1 or GFAP was determined by immunofluorescence double staining. Results: Compared with the control group, the escape latency of rats in the noise group was increased by 16.29 s, 17.71 s, and 20.26 s on days 3, 4, and 5, respectively. On day 6, the noise-exposed rats spent shorter time in the target quadrant and had fewer times in crossing the platform[ (7.25±2.27) s and (1.13±0.64) times] than the control group[ (15.64±3.99) s and (4.25±2.12) times] (P<0.05) . After noise exposure, hippocampal neurons of rats displayed marked nuclear hyperchromatic and pyknosis phenomenon. The noise-exposed rats had higher numbers of both microglia and astrocytes (27.00±2.65 and 43.33±5.51) in the DG area of the hippocampus relative to the control group (14.67±3.06 and 20.00±4.58) (P<0.05) . Moreover, the glial cells in the noise group had larger cell cytosol with more and thicker branches. The protein expression levels of inflammatory cytokines Cleaved-IL-1β and Cleaved-IL-18 in the hippocampus of rats in the noise group (1.55±0.19 and 1.74±0.12) were significantly higher than the control group (1.00±0.11 and 1.00±0.13) (P<0.05) . After noise exposure, the protein expression levels of AIM2, Cleaved-Caspase-1 and ASC (1.19±0.09, 1.34±0.07 and 1.14±0.01) were higher than the control group (1.00±0.07, 1.00±0.14 and 1.00±0.06) and differences between the two groups were statistically significant (P<0.05) . A significant increase in the number of cells co-localizing AIM2 with Iba-1 or GFAP in the noise group (28.67±4.04 and 40.67±5.13) compared with the control group (15.67±4.04 and 17.67±3.79) , and statistically significant differences were observed between the two groups (P<0.05) . Conclusion: Noise exposure may activate the AIM2 inflammasome in hippocampal glial cells of rats, releasing excessive inflammatory cytokines and causing neuroinflammation that damages neurons.
目的： 探讨噪声接触导致大鼠认知功能障碍中黑色素瘤缺乏因子2（AIM2）的作用。 方法： 于2023年4月，将16只雄性Wistar大鼠随机分为对照组和噪声组，每组8只。噪声组大鼠置于50 cm×50 cm×40 cm的透明箱子中，每天施加声压级100 dB（A）的白噪声4 h，连续30 d。对照组大鼠置于相同的箱子中，环境噪声<60 dB（A）。30 d噪声接触完成后，用Morris水迷宫实验测试大鼠的学习和记忆功能；苏木精-伊红（HE）染色观察海马组织的病理形态变化；Western blot检测AIM2、胱天蛋白酶-1 （Caspase-1）、凋亡相关斑点样蛋白（ASC）、白细胞介素（IL）-1β、IL-18、离子钙结合衔接分子-1（Iba-1）和胶质纤维酸性蛋白（GFAP）的蛋白表达水平；免疫组化染色观察海马组织中Iba-1和GFAP的表达情况；免疫荧光双染测定AIM2与Iba-1或GFAP的共定位情况。 结果： 与对照组比较，噪声组大鼠在第3、4、5天的逃避潜伏期分别增加了16.29、17.71、20.26 s。第6天噪声组大鼠停留在目标象限的时间[（7.25±2.27）s]和穿越平台的次数[（1.13±0.64）次]明显低于对照组[（15.64±3.99）s和（4.25±2.12）次]（P<0.05）。噪声组大鼠海马齿状回（DG）区小胶质细胞和星形胶质细胞数量（27.00±2.65和43.33±5.51）明显高于对照组（14.67±3.06和20.00±4.58）（P<0.05），且细胞胞体变大、分支数量增加且变粗。噪声组大鼠海马的炎症因子裂解（Cleaved）-IL-1β和Cleaved-IL-18的蛋白表达水平（1.55±0.19和1.74±0.12）明显高于对照组（1.00±0.11和1.00±0.13）（P<0.05）。噪声组大鼠海马的AIM2、Cleaved-Caspase-1和ASC蛋白表达水平（1.19±0.09、1.34±0.07和1.14±0.01）高于对照组（1.00±0.07、1.00±0.14和1.00±0.06）（P<0.05）。噪声组大鼠海马中AIM2与Iba-1或GFAP共定位细胞数量（28.67±4.04和40.67±5.13）明显高于对照组（15.67±4.04和17.67±3.79）（P<0.05）。 结论： 噪声接触可能会激活大鼠海马神经胶质细胞中的AIM2炎症小体，释放大量的炎症因子，引起神经炎症损伤神经元。.
目的： 探讨噪声接触导致大鼠认知功能障碍中黑色素瘤缺乏因子2（AIM2）的作用。 方法： 于2023年4月，将16只雄性Wistar大鼠随机分为对照组和噪声组，每组8只。噪声组大鼠置于50 cm×50 cm×40 cm的透明箱子中，每天施加声压级100 dB（A）的白噪声4 h，连续30 d。对照组大鼠置于相同的箱子中，环境噪声<60 dB（A）。30 d噪声接触完成后，用Morris水迷宫实验测试大鼠的学习和记忆功能；苏木精-伊红（HE）染色观察海马组织的病理形态变化；Western blot检测AIM2、胱天蛋白酶-1 （Caspase-1）、凋亡相关斑点样蛋白（ASC）、白细胞介素（IL）-1β、IL-18、离子钙结合衔接分子-1（Iba-1）和胶质纤维酸性蛋白（GFAP）的蛋白表达水平；免疫组化染色观察海马组织中Iba-1和GFAP的表达情况；免疫荧光双染测定AIM2与Iba-1或GFAP的共定位情况。 结果： 与对照组比较，噪声组大鼠在第3、4、5天的逃避潜伏期分别增加了16.29、17.71、20.26 s。第6天噪声组大鼠停留在目标象限的时间[（7.25±2.27）s]和穿越平台的次数[（1.13±0.64）次]明显低于对照组[（15.64±3.99）s和（4.25±2.12）次]（P<0.05）。噪声组大鼠海马齿状回（DG）区小胶质细胞和星形胶质细胞数量（27.00±2.65和43.33±5.51）明显高于对照组（14.67±3.06和20.00±4.58）（P<0.05），且细胞胞体变大、分支数量增加且变粗。噪声组大鼠海马的炎症因子裂解（Cleaved）-IL-1β和Cleaved-IL-18的蛋白表达水平（1.55±0.19和1.74±0.12）明显高于对照组（1.00±0.11和1.00±0.13）（P<0.05）。噪声组大鼠海马的AIM2、Cleaved-Caspase-1和ASC蛋白表达水平（1.19±0.09、1.34±0.07和1.14±0.01）高于对照组（1.00±0.07、1.00±0.14和1.00±0.06）（P<0.05）。噪声组大鼠海马中AIM2与Iba-1或GFAP共定位细胞数量（28.67±4.04和40.67±5.13）明显高于对照组（15.67±4.04和17.67±3.79）（P<0.05）。 结论： 噪声接触可能会激活大鼠海马神经胶质细胞中的AIM2炎症小体，释放大量的炎症因子，引起神经炎症损伤神经元。.
摘要：
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