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[The effect of the AIM2 inflammasome in noise-induced cognitive dysfunction in rats]
1Institute of Occupational and Environmental Health, Twelfth People's Hospital Affiliated to Guangzhou Medical University, Guangzhou 510620, China.
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.
Insights
Noise exposure triggers absent in melanoma 2 (AIM2) inflammasome activation in rat hippocampal glial cells, leading to neuroinflammation and cognitive deficits. This study reveals AIM2
Area of Science:
- Neuroscience
- Toxicology
- Immunology
Background:
- Chronic noise exposure is a growing concern for cognitive health.
- Neuroinflammation is implicated in various cognitive dysfunctions.
- The role of the AIM2 inflammasome in noise-induced cognitive impairment requires further investigation.
Purpose of the Study:
- To investigate the role of absent in melanoma 2 (AIM2) inflammasome-mediated neuroinflammation in rats subjected to noise-induced cognitive dysfunction.
- To elucidate the molecular mechanisms underlying noise-induced cognitive impairment.
Main Methods:
- Wistar rats were exposed to 100 dB (A) white noise for 30 days.
- Cognitive function was assessed using the Morris water maze.
- Hippocampal tissues were analyzed for neuronal morphology, glial cell activation (Iba-1, GFAP), and expression of AIM2, caspase-1, ASC, IL-1β, and IL-18 via Western blot, HE staining, and immunofluorescence.
Main Results:
- Noise-exposed rats exhibited impaired learning and memory, characterized by increased escape latency and reduced time in the target quadrant.
- Significant neuronal damage, increased microgliosis and astrogliosis, and elevated levels of AIM2, caspase-1, ASC, IL-1β, and IL-18 were observed in the hippocampus.
- AIM2 co-localization with microglia (Iba-1) and astrocytes (GFAP) was significantly increased in noise-exposed rats.
Conclusions:
- Noise exposure activates the AIM2 inflammasome in hippocampal glial cells.
- This activation leads to the release of inflammatory cytokines, causing neuroinflammation and neuronal damage.
- The AIM2 inflammasome pathway is a critical mediator of noise-induced cognitive dysfunction.
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