Mechanisms of tissue damage in Huntington’s disease involve excitotoxicity, mitochondrial damage, and neuroinflammation, including microglia activation. In the present study, we investigate the role of pyroptosis process in the striatal neurons of the R6/2 mouse model of Huntington’s disease. Transgenic mice were sacrificed at 4 and 13 weeks of age. After sacrifice, histological and immunohistochemical studies were performed. We found that NLRP3 and Caspase-1 were intensely expressed in 13-week-old R6/2 mice. Moreover, NLRP3 expression levels were higher in striatal spiny projection neurons and in parvalbumin interneurons, which are prone to degenerate in HD.

亨廷顿病的组织损伤机制涉及兴奋性毒性、线粒体损伤和神经炎症，包括小胶质细胞激活。在本研究中，我们研究了亨廷顿病 R6/2 小鼠模型纹状体神经元焦亡过程的作用。转基因小鼠在4周龄和13周龄时被处死。处死后，进行组织学和免疫组织化学研究。我们发现 NLRP3 和 Caspase-1 在 13 周龄的 R6/2 小鼠中强烈表达。此外，NLRP3 在纹状体棘投射神经元和小白蛋白中间神经元中表达水平较高，这些神经元在 HD 中容易退化。