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experiments. A mechanistic study revealed that crocetin significantly promoted the differentiation of primary cultured oligodendrocyte precursor cells to oligodendrocytes through up-regulation of nuclear Ki67 and transcription factor 2 (Olig2). Oligodendrocytes, the myelin-forming cells, have been reported to be lifelong partners of neurons. Therefore, to investigate the effects of crocetin on myelin and neurons, lysophosphatidylcholine (LPC)-treated primary mixed midbrain neuronal/glial culture was used. Immunofluorescence results indicated that crocetin treatment protected neurons and suppressed microglial activation against LPC-induced injury. To further discern the effects of GJ-4 on white matter injury and neuroinflammation, an LPC-induced mouse model was developed. GJ-4 administration increased oligodendrocyte proliferation, differentiation, and myelin repair. The mechanistic study indicated that GJ-4 improved white matter injury through the regulation of neuroinflammatory dysfunction. These data indicated that GJ-4 effectively repaired white matter damage in the LPC-treated mice. Thus, the present study supported GJ-4 as a potential therapeutic agent for AD and white matter related diseases.
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Zang et al. (2022) studied this question.
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