The present study aimed to explore the effects of n-3 polyunsaturated fatty acids (PUFAs) on autophagy and their potential for promoting locomotor recovery after spinal cord injury (SCI). Primary neurons were isolated and cultured. Sprague-Dawley rats were randomly divided into three groups and fed diets with different amounts of n-3 PUFAs. A model of spinal cord contusion was created at the T10 spinal segment and the composition of PUFAs was analyzed using gas chromatography. Spinal repair and motor function were evaluated postoperatively. Assessment of the effects of n-3 PUFAs on autophagy and mammalian target of rapamycin complex 1 (mTORC1) was performed using immunofluorescence staining and western blotting. In vitro, n-3 PUFAs inhibited mTORC1 and enhanced autophagy. The n-3 PUFA levels and the ratio of n-3 PUFA to n-6 PUFA in the spinal cord and serum of rats fed a high-n-3 PUFA diet were higher before and after operation (P<0.05). Additionally, rats in the high-n-3 PUFA group showed improved motor function recovery, spinal cord repair-related protein expression level (MBP, Galc and GFAP). Expression levels if these protiens in the high-n-3 PUFA diet group expressed the highest levels, followed by the low-n-3 PUFA diet group and finally the control group (P<0.05). high-n-3 PUFA diet promoted autophagy ability and inhibited activity of the mTORC1 signaling pathway compared with the low-n-3 PUFA diet group or the control group (P<0.05). These results suggest that exogenous dietary n-3 PUFAs can inhibit mTORC1 signaling and enhance autophagy, promoting functional recovery of rats with SCI.
The canonical Wnt pathway is vital to bone physiology by increasing bone mass through elevated osteoblast survival. Although investigated extensively in stem cells, its role in osteoblastic MC3T3-E1 cells has not been completely determined. To explore how this pathway is regulated by different conditions, we assessed the anti-apoptotic effects of substance P on the canonical Wnt pathway in MC3T3-E1 cells by treating cells with serum deprivation or serum starving with "substance P," a neuropeptide demonstrated to promote bone growth and stimulate Wnt signaling. The results showed that serum deprivation both induced apoptosis and activated Wnt signal transduction while substance P further stimulated the Wnt pathway via the NK-1 receptor but protected the cells from apoptotic death. Fast-tracking of Wnt signaling by substance P was also noted. These results indicate that nutritional deprivation and substance P synergistically activated the canonical Wnt pathway, a finding that helps to reveal the role of Wnt signaling in bone physiology affected by nutritional deprivation and neuropeptide substance P.
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