This aim of the study was to investigate the effect of CYP1A2 gene polymorphism on the metabolism of theophylline in minority and Han nationality. A total of 50 cases of Han (Han group) and 50 minority nationalities (ethnic groups) treated with theophylline were selected for the study. The genotype and allele frequencies of the two groups of CYP1A2 gene, G-3113A and G-3860A, were compared to determine the rate of theophylline clearance. The results showed that there was no significant difference in the concentration of the homeostasis and the rate of the theophylline removal rate (P>0.05). There was no significant difference in the genotype and allele frequencies of the CYP1A2 gene, G-3113A and G-3860A apolymorphic site. This study employed a logarithm to determine theophylline clearance in order to correlate it with the normal distribution. The results showed that the theophylline clearance of the two groups of CYP1A2 G-3113A gene loci A allele carriers (AA+GA genotype) was significantly lower than that of the G allele carriers (GG genotype), and a significant difference between the groups was identified (P<0.05). There was no significant difference in the theophylline clearance rates in the two groups for the CYP1A2 gene, G-3860A apolymorphic site (P>0.05). Compared to the GG genotype of the CYP1A2 gene, the G-3113A site AA and GA genotype patients had a low clearance rate in the theophylline, whereas there was no correlation between teh genotypes of the CYP1A2 gene, G-3860A and the rate of theophylline clearance.
Parecoxib, a non-steroidal anti-inflammatory drug, has been reported to possess protective effects against sepsis. However, its detailed role and underlying mechanisms in septic cardiomyopathy remain unclear. Therefore, the goal of the present study was to clarify the function and to investigate the mechanisms of parecoxib in lipopolysaccharide (LPS)-treated H9c2 rat cardiomyocytes. TNF-α, IL-1β and IL-6 expression levels in parecoxib-treated H9c2 cells stimulated with LPS were assessed using ELISA. Parecoxib-treated H9c2 cells stimulated with LPS were tested for viability using the Cell Counting Kit-8 assay. Western blotting analysis and 5-ethynyl-2'-deoxyuridine were used to evaluate cell proliferation. Apoptosis was assessed using TUNEL and western blotting. To assess the protein expression of the MAPK signaling pathway, western blotting was performed. The data showed that parecoxib significantly and dose-dependently reduced the inflammatory responses of LPS-treated H9c2 cells. Parecoxib also significantly and dose-dependently increased the proliferation and inhibited the apoptosis of LPS-treated H9c2 cells. In addition, parecoxib significantly suppressed the activation of the MAPK (p38, JNK and ERK) signaling pathway. The current study indicated that parecoxib could be a viable therapeutic option for septic cardiomyopathy.
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