Sodium tanshinone IIA sulfonate promotes proliferation and differentiation of endogenous neural stem cells to repair rat spinal cord injury via the Notch pathway

Spinal cord injury (SCI) is a severe neurological disorder that can lead to sensory and motor impairments. Current treatments can only alleviate symptoms and reduce complications, but no definitive cure exists. Therefore, developing regenerative strategies that promote the proliferation and neuronal differentiation of ENSCs holds significant potential. Tanshinone IIA (TIIA) has extensive neuroprotective effects. Sodium tanshinone IIA sulfonate (STS), a derivative of TIIA, significantly enhances water solubility, making it easier to prepare injectable formulations and increasing bioavailability. The effects of STS on the proliferation and differentiation of neural stem cells (NSCs) after SCI remain unclear and require further exploration. Experiments were designed to determine whether STS can regulate the proliferation and differentiation of ENSCs post-SCI and to preliminarily elucidate its mechanism of action. The regulatory effects of STS on NSCs may be achieved by inhibiting the excessive activation of the Notch signaling pathway post-SCI. This finding provides new insights into the treatment of SCI.

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  STS significantly reduced the levels of inflammatory indices in the LPS-induced rats NSCs inflammation model and improved the viability of rats NSCs following inflammatory injury.
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  STS also significantly increased the proliferation of NSCs and their differentiation into neurons while reducing their differentiation into astrocytes.
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  In vivo, STS markedly improved the hindlimb motor function of rats with SCI, decreased the levels of pro-inflammatory factors IL-6 and TNF-α, and increased the level of the anti-inflammatory factor IL-10, thereby improving the pathological morphology of the injured spinal cord in rats post-SCI.