Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although several studies have demonstrated the neuroprotective effects of Hericium erinaceus (H.E.), its mechanisms in cerebellar ataxia remain largely unknown. Here, we investigated the neuroprotective effects of H.E. treatment in an animal model of 3-acetylpyridine (3-AP)-induced cerebellar ataxia. Animals administered 3-AP injection exhibited remarkable impairments in motor coordination and balance. There were no significant effects of 25 mg/kg H.E. on the 3-AP treatment group compared to the 3-AP saline group. Interestingly, there was also no significant difference in the 3-AP treatment group compared to the non-3-AP control, indicating a potential rescue of motor deficits. Our results revealed that 25 mg/kg H.E. normalised the neuroplasticity-related gene expression to the level of non-3-AP control. These findings were further supported by increased protein expressions of pERK1/2-pCREB-PSD95 as well as neuroprotective effects on cerebellar Purkinje cells in the 3-AP treatment group compared to the 3-AP saline group. In conclusion, our findings suggest that H.E. potentially rescued behavioural motor deficits through the neuroprotective mechanisms of ERK-CREB-PSD95 in an animal model of 3-AP-induced cerebellar ataxia.

小脑性共济失调是一种神经退行性疾病，没有明确的治疗方法。虽然一些研究已经证明猴头菇的神经保护作用（HE），其在小脑性共济失调中的机制在很大程度上仍然未知。在这里，我们研究了 HE 治疗在 3-乙酰吡啶 (3-AP) 诱导的小脑共济失调动物模型中的神经保护作用。给予 3-AP 注射的动物在运动协调和平衡方面表现出显着的损害。与 3-AP 盐水组相比，25 mg/kg HE 对 3-AP 治疗组没有显着影响。有趣的是，与非 3-AP 对照组相比，3-AP 治疗组也没有显着差异，表明运动缺陷的潜在挽救。我们的结果显示，25 mg/kg HE 使神经可塑性相关基因表达正常化至非 3-AP 对照水平。与 3-AP 盐水组相比，3-AP 治疗组中 pERK1/2-pCREB-PSD95 的蛋白表达增加以及对小脑浦肯野细胞的神经保护作用进一步支持了这些发现。总之，我们的研究结果表明，在 3-AP 诱导的小脑共济失调的动物模型中，HE 可能通过 ERK-CREB-PSD95 的神经保护机制挽救了行为运动缺陷。