AimsRecovery after peripheral nerve injury (PNI) is often difficult, and there is no optimal treatment. Schwann cells (SCs) are important for peripheral nerve regeneration, so SC‐targeting treatments have gained importance. Adipose‐derived stem cells (ADSCs) and their exosomes can promote peripheral nerve repair, but their interactions with SCs are unclear.MethodsPurified SCs from sciatic nerve injury sites were harvested, and apoptosis and proliferation of SCs at post‐PNI 24 hours were analyzed. The effects of coculture with ADSCs and different concentrations of ADSC‐derived exosomes (ADSC‐Exo) were studied through in vitro experiments by flow cytometry, CCK8 assay, immunofluorescence staining, and histological analysis. The expression of the apoptosis‐related genes Bcl‐2 and Bax was also analyzed by qRT‐PCR.ResultsADSC‐Exo reduced the apoptosis of SCs after PNI by upregulating the anti‐apoptotic Bcl‐2 mRNA expression and downregulating the pro‐apoptotic Bax mRNA expression. Further, it also improved the proliferation rate of SCs. This effect was confirmed by the morphological and histological findings in PNI model rats.ConclusionOur results present a novel exosome‐mediated mechanism for ADSC‐SC cross talk that reduces the apoptosis and promotes the proliferation of SCs and may have therapeutic potential in the future.

All-inorganic cesium lead halide perovskite nanocrystals (IPNCs) exhibit exceptional optical properties but the low chemical and structural stability has restricted their longterm applications. According to previous studies, hybridization of IPNCs with other matrix materials provides an efficient method for improving their optical stability. Here, we develop a new strategy to synthesize a chemically and structurally stable CsPbBr 3 perovskite material using polymer nanofiber as the [a]

The aim of the present study was to determine whether arcuate nucleus (ARC) lesions affect the ghrelin level in the plasma and the stomach in monosodium glutamate (MSG)‑treated mice. The aim of the present study was to investigate whether the ARC was destroyed in mice treated neonatally with MSG, and whether the ARC lesions affect the ghrelin level in the plasma and lipid mobilization in MSG‑treated mice. The results revealed that MSG led to a marked reduction in ARC cresyl violet staining, tyrosine hydroxylase-immunoreactive (IR) neurons and neuropeptide Y‑IR fibers, compared with saline controls. MSG‑treated mice exhibited significantly increased body mass compared with saline controls, and MSG treatment did not prevent food deprivation‑induced decrease in white adipose tissue mass compared with controls. Plasma ghrelin levels were significantly increased in MSG‑treated mice that were fasted for 48 h, compared with the levels prior to fasting and re‑feeding, and the preprandial peak of plasma ghrelin persisted in MSG‑treated mice. In summary, the ARC was not found to be essential for food deprivation‑induced lipid mobilization and preprandial peak in MSG‑treated mice. However, this finding does not mean that ARC neurons do not contribute to food sensing and lipid mobilization under normal conditions, as compensatory mechanisms may have emerged after the ablation of ARC neurons.