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Purpose@#The main treatment options of neurogenic bladder remains catheterization and long-term oral medications. Metabolic interventions have shown good therapeutic results in many diseases. To date, no studies have characterized the metabolites of the detrusor muscle during neurogenic bladder. Using metabolomics, new muscle metabolomic signatures were identified to reveal the temporal metabolic profile of muscle during disease progression. @*Methods@#We used 42 Sprague-Dawley rats (200±20 g, males) for T10 segmental spinal cord injury modeling and collected detrusor tissue and performed nontargeted metabolomics after sham surgery, 30-minute, 6-hour, 12-hour, 24-hour, 5-day, and 2-week postmodelling, to identify the dysregulated metabolic pathways and key metabolites. @*Results@#By comparing mzCloud, mzVault, MassList, we identified a total of 1,271 metabolites and enriched a total of 12 metabolism-related pathways with significant differences (P<0.05) based on Kyoto Encyclopedia of Genes and Genomes analysis. Metabolites in several differential metabolic pathways such as ascorbate and aldarate metabolism, Steroid hormone biosynthesis, and carbon metabolism are altered in a regular manner before and after ridge shock. @*Conclusions@#Our study is the first time-based metabolomic study of rat forced urinary muscle after traumatic spinal cord injury, and we identified multiple differential metabolic pathways during injury that may improve long-term management strategies for neurogenic bladder and reduce costs in long-term treatment.
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<p><b>OBJECTIVE</b>To observe the expression of P-selectin in the penile vascular epithelial cells and the morphological changes in the ultrastructure of the penile cavernous tissues of smoking rats, and to explore the pathogenesis of smoking-induced erectile dysfunction.</p><p><b>METHODS</b>Fifty healthy Wistar rats were randomly divided into a normal control, a long-term heavy smoking group, a long-term light smoking, a short-term heavy smoking and a smoking cessation group. Their erectile function was tested by subcutaneous injection of apomorphine (APO), the P-selectin expression in the penile vascular epithelial cells detected by ELISA and the morphological changes in the ultrastructure of the penile cavernous tissues observed under the transmission electron microscope (TEM).</p><p><b>RESULTS</b>The levels of P-selectin were 10.78 +/- 1.71 ng/L, 62.62 +/- 5.95 ng/L, 40.06 +/- 3.97 ng/L, 41.37 +/- 4.06 ng/L and 22.80 +/- 3.15 ng/L respectively in the normal control, long-term heavy smoking, long-term light smoking, short-term heavy smoking and smoking cessation groups, with significant differences between the control group and the other four (P < 0.05). Electron microscopy showed abnormal arrangement of endothelia, penile cavernous sinuses and smooth muscle cells, disrupted continuity of endothelia, damaged ultrastructure of endothelial and smooth muscle cells in the penile cavernous tissue, and obvious proliferation and fibrosis of interstitial tissues in the smoking rats.</p><p><b>CONCLUSION</b>Smoking increases the P-selectin expression in the penile vascular epithelial cells and damages the ultrastructure of the penile cavernous tissue, which may be the main contributors to smoking-induced erectile dysfunction.</p>