ABSTRACT
Ketamine abuse has dramatically increased in recently years. With the widely application of ketamine, its side effects, especially cystitis induced by long-term use, have attracted more and more attention from the public. In the present study, we aimed to explore the potential generative mechanism of ketamine-induced cystitis by determining the endogenous metabolites at different time points after ketamine treatment. Body weight, bladder/body coefficient, urinary frequency, urinary potassium, serum IL-6, and TNF-α were determined at different time points after ketamine treatment. H&E staining was used to observe the changes of histopathology. Metabonomics was performed to determine the changes of endogenous metabolites. After 12 weeks of treatment, obvious inflammatory reaction was noticed in the KET group; the body weight and urinary potassium of the KET group were significantly lower than the NS group (P < 0.05) and other factors, such as urinary frequency, bladder/body coefficient, serum TNF-α and IL-6 were higher than the NS group (P < 0.05). A total of 30, 28, and 32 significantly changed metabolites were identified at the 1st week, 4th week and 12th week, respectively. Metabolic pathway analysis showed that different metabolic pathways were affected during the treatment process. Linoleic acid metabolism, beta-alanine metabolism, glyoxylate and dicarboxylate metabolism were only affected following long-term administration of ketamine. Those metabolic pathways may have a close relationship with cystitis induced by ketamine.
ABSTRACT
OBJECTIVE: To observe the expression of phosphatase and tensin homology deleted on chromosome ten (PTEN) in myocardial tissue in patients with coronary heart disease, and explore the relevance between the expression of PTEN and the occurrence and development of coronary heart disease. METHODS: A total of 16 death cases with pathological diagnosis of coronary heart disease were collected as experimental group, and 19 cases without myocardial lesions were selected as control group. The expression of PTEN protein and its mRNA were detected by immunohistochemistry and real-time fluorescence quantitative PCR respectively. The correlation between the expression of PTEN and the pathogenesis of coronary heart disease was analyzed. RESULTS: The expression of PTEN protein in myocardium in cases with coronary heart disease was significantly lower compared with the control group (P < 0.05). There was no statistical difference of the expression of PTEN mRNA between experimental and control group (P > 0.05). CONCLUSION: PTEN may be involved in the occurrence and development of coronary heart disease.
