To investigate the sex-dependent differentiation of Sox10 cells and their response to pathological conditions such as lipopolysaccharide (LPS) exposure or ischemia, we utilized Sox10 Cre-ER T2 , tdTomato mice. Tamoxifen administration induced the expression of red fluorescent protein (RFP) in these cells, facilitating their subsequent tracking and analysis after LPS injection and ischemia via immunofluorescence staining. Propidium iodide (PI) was injected to label necrotic cells following LPS administration. We found that the conversion of Sox10 cells to pericytes in female mice was significantly higher than in male mice, especially in those exposed to LPS. After LPS injection, the number of PI + necrotic cells were significantly greater in females than in males. Moreover, RFP + cells did not co-localize with glial fibrillary acidic protein (GFAP) or cluster of differentiation 11b (CD11b). Similarly, after brain ischemia, RFP + cells did not express cluster of differentiation 13 (CD13), neuronal nuclei (NeuN), GFAP, or ionised calcium binding adaptor molecule 1 (Iba-1). These findings indicate that the conversion of Sox10 cells to pericytes following LPS exposure is sex-dependent, with neither male nor female groups showing differentiation into other cell types after LPS exposure or under ischemic conditions. The differences in LPS-induced necrosis of pericytes between sexes may explain the variations in the conversion of Sox10 cells to pericytes in both sexes.
Yu Wen,Zuxian Zhang,Zhongmou Cai,Baoning Liu,Zhehao Wu,Yude Liu
Our team’s pharmacological and clinical trials proved that ligustrazine/borneol spray had a definite effect on ischemic stroke (IS). To solve the shortcomings of ligustrazine/borneol spray, such as low bioavailability, short half-life, and poor compatibility between borneol and ligustrazine, ligustrazine-loaded borneol liposomes (LIP@TMP) were successfully prepared by a thin-film ultrasonication method. The average particle size of LIP@TMP was 282.4 ± 3.6 nm, the drug loading rate was 14.5 ± 0.6%, and the entrapment efficiency was 42.7 ± 1.0%, which had excellent stability and sustained release ability. In addition, live/dead fluorescent staining and the CCK-8 test confirmed that LIP@TMP had good biocompatibility. Moreover, middle cerebral artery occlusion (MCAO) rat model experiments further demonstrated that LIP@TMP could significantly alleviate cerebral ischemia and reperfusion injury by improving neurological scores, reducing cerebral infarct volume, promoting neurogenesis, inhibiting inflammation, and reducing tissue damage. In addition, LIP@TMP enhanced neuronal marker doublecortin (DCX) and neuronal nuclei (NEUN), inhibited inflammatory factors (TNF-α and IL-1β), and reduced apoptosis signal molecules (TUNEL and caspase-3). The findings of this study suggested that the prepared LIP@TMP had tremendous potential for the treatment of cerebral ischemia.
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