目的观察扶正解毒汤辅治脓毒症休克(septic shock,SS)的效果及对炎性因子和可溶性白细胞分化抗原14(soluble cluster of differentiation antigen 14,sCD14)、高迁移率族蛋白1(high mobility group box 1,HMGB1)水平的影响。方法选取201...目的观察扶正解毒汤辅治脓毒症休克(septic shock,SS)的效果及对炎性因子和可溶性白细胞分化抗原14(soluble cluster of differentiation antigen 14,sCD14)、高迁移率族蛋白1(high mobility group box 1,HMGB1)水平的影响。方法选取2018年3月—2022年3月本院接诊的SS患者109例,以随机数字表法分为常规组54例(常规治疗)、联合组55例(常规治疗联合扶正解毒汤)。检测炎性因子[超敏C反应蛋白(hypersensitive C-reactive protein,hs-CRP)、降钙素原(procalcitonin,PCT)]、sCD14、HMGB1、急性生理与慢性健康评分(acute physiology and chronic health evaluationⅡ,APACHEⅡ)、ICU入住时间、临床疗效、安全性变化。结果治疗后,两组血清hs-CRP、PCT、sCD14、HMGB1水平及APACHEⅡ评分均降低,以联合组更明显(P<0.05)。联合组ICU入住时间短于常规组(P<0.05)。联合组临床总有效率高于常规组(P<0.05)。常规组与联合组肝肾功能异常、血小板损伤、皮疹、呕吐、腹泻发生率比较,差异无统计学意义(P>0.05)。结论扶正解毒汤可减轻SS患者炎症反应及危重症状,降低sCD14、HMGB1水平,加快恢复速度,提高临床疗效,且安全可靠。展开更多
<strong>Introduction:</strong> Krüppel Like Factor 14 (KLF14) gene has recently been identified as a master gene for multiple metabolic phenotypes. The aim of the research study was to investigate the...<strong>Introduction:</strong> Krüppel Like Factor 14 (KLF14) gene has recently been identified as a master gene for multiple metabolic phenotypes. The aim of the research study was to investigate the relationship between KLF14 rs4731702 (C/T) gene polymorphism with Type 2 Diabetes Mellitus (T2DM) in a Cameroonian population. <strong>Patients and Methods:</strong> This case-control study was conducted in 85 patients with T2DM and 95 healthy normoglycemic controls. All were nonrelated, of Cameroonian origin, and were adults aged 24 years old and above. Demographic, clinical and biological data were collected, and biochemical explorations were performed using enzymatic colorimetric methods. The genotyping of KLF14 rs4731702 (CT) gene polymorphism was done by the Polymerase Chain Reaction and Restriction Fragment Length Polymorphism. Results: In comparing the Cameroonian population that consisted of 85 patients with T2DM and 95 healthy controls, the minor or risk allele of the rs4731702 (C/T) polymorphism of the KLF14 gene was T (63.53% diabetic patients vs. 26.32% healthy controls, OR = 4.877 and p < 0.0001) while the protective allele was C (36.47% diabetic patients vs. 73.68% healthy controls, OR = 0.205 and p < 0.0001). The susceptibility to T2DM was higher among subjects having the CT and TT genotypes with OR = 2.721 and p = 0.0145) and OR = 3.907 and p < 0.0001) respectively. This gene polymorphism was not preferentially associated with a specific diabetes phenotype. <strong>Conclusion:</strong> This study has demonstrated for the first time the relationship between the KLF14 rs4731702 (C/T) gene polymorphism and T2DM in this Cameroonian population. This gene polymorphism could be a promising target for personalized medicine through the development of clinical genetic testing.展开更多
Objective: To explore whether METTL14 is involved in regulating the fibroblast proliferation and inflammatory cytokine secretion by regulating the m6A modification of pri‑miR‑141. Methods: MRC‑5 cells were transfected...Objective: To explore whether METTL14 is involved in regulating the fibroblast proliferation and inflammatory cytokine secretion by regulating the m6A modification of pri‑miR‑141. Methods: MRC‑5 cells were transfected via METTL14 overexpression lentivirus to increase METTL14 expression. Levels of METTL14 and ZEB1 were measured by qPCR and western blot. The effect of METTL14 on MRC‑5 proliferation and apoptosis was determined by CCK‑8 and flow cytometry, respectively. The ELISA kits of IL‑2, IL6 and TNF‑α were used to detect the effect of METTL14 on MRC‑5 inflammatory secretion. m6A modification site on pri‑miR‑141 was detected by meRIP. The binding site between pri‑miR‑141 and METTL14 was determined by RIP. Results: We successfully upregulated METTL14 expression in MRC‑5 cells. Elevated METTL14 promoted MRC‑5 cell proliferation, suppressed its apoptosis and promoted inflammatory factors secretion in MRC‑5 cells. pri‑miR‑141 had m6A modification sites. pri‑miR‑141 can directly bind to METTL14. METTL14 upregulation increased miR‑141 while suppressed ZEB1 expression. Conclusion: METTL14 can promote the expression of miR‑141 by increasing the m6A modification site of pri‑miR‑141, and inhibit ZEB1, thereby promoting the proliferation of fibroblasts and the secretion of inflammatory factors.展开更多
文摘目的观察扶正解毒汤辅治脓毒症休克(septic shock,SS)的效果及对炎性因子和可溶性白细胞分化抗原14(soluble cluster of differentiation antigen 14,sCD14)、高迁移率族蛋白1(high mobility group box 1,HMGB1)水平的影响。方法选取2018年3月—2022年3月本院接诊的SS患者109例,以随机数字表法分为常规组54例(常规治疗)、联合组55例(常规治疗联合扶正解毒汤)。检测炎性因子[超敏C反应蛋白(hypersensitive C-reactive protein,hs-CRP)、降钙素原(procalcitonin,PCT)]、sCD14、HMGB1、急性生理与慢性健康评分(acute physiology and chronic health evaluationⅡ,APACHEⅡ)、ICU入住时间、临床疗效、安全性变化。结果治疗后,两组血清hs-CRP、PCT、sCD14、HMGB1水平及APACHEⅡ评分均降低,以联合组更明显(P<0.05)。联合组ICU入住时间短于常规组(P<0.05)。联合组临床总有效率高于常规组(P<0.05)。常规组与联合组肝肾功能异常、血小板损伤、皮疹、呕吐、腹泻发生率比较,差异无统计学意义(P>0.05)。结论扶正解毒汤可减轻SS患者炎症反应及危重症状,降低sCD14、HMGB1水平,加快恢复速度,提高临床疗效,且安全可靠。
文摘<strong>Introduction:</strong> Krüppel Like Factor 14 (KLF14) gene has recently been identified as a master gene for multiple metabolic phenotypes. The aim of the research study was to investigate the relationship between KLF14 rs4731702 (C/T) gene polymorphism with Type 2 Diabetes Mellitus (T2DM) in a Cameroonian population. <strong>Patients and Methods:</strong> This case-control study was conducted in 85 patients with T2DM and 95 healthy normoglycemic controls. All were nonrelated, of Cameroonian origin, and were adults aged 24 years old and above. Demographic, clinical and biological data were collected, and biochemical explorations were performed using enzymatic colorimetric methods. The genotyping of KLF14 rs4731702 (CT) gene polymorphism was done by the Polymerase Chain Reaction and Restriction Fragment Length Polymorphism. Results: In comparing the Cameroonian population that consisted of 85 patients with T2DM and 95 healthy controls, the minor or risk allele of the rs4731702 (C/T) polymorphism of the KLF14 gene was T (63.53% diabetic patients vs. 26.32% healthy controls, OR = 4.877 and p < 0.0001) while the protective allele was C (36.47% diabetic patients vs. 73.68% healthy controls, OR = 0.205 and p < 0.0001). The susceptibility to T2DM was higher among subjects having the CT and TT genotypes with OR = 2.721 and p = 0.0145) and OR = 3.907 and p < 0.0001) respectively. This gene polymorphism was not preferentially associated with a specific diabetes phenotype. <strong>Conclusion:</strong> This study has demonstrated for the first time the relationship between the KLF14 rs4731702 (C/T) gene polymorphism and T2DM in this Cameroonian population. This gene polymorphism could be a promising target for personalized medicine through the development of clinical genetic testing.
基金Health Industry Scientific Research Project of Hainan Province (No.21A200259)。
文摘Objective: To explore whether METTL14 is involved in regulating the fibroblast proliferation and inflammatory cytokine secretion by regulating the m6A modification of pri‑miR‑141. Methods: MRC‑5 cells were transfected via METTL14 overexpression lentivirus to increase METTL14 expression. Levels of METTL14 and ZEB1 were measured by qPCR and western blot. The effect of METTL14 on MRC‑5 proliferation and apoptosis was determined by CCK‑8 and flow cytometry, respectively. The ELISA kits of IL‑2, IL6 and TNF‑α were used to detect the effect of METTL14 on MRC‑5 inflammatory secretion. m6A modification site on pri‑miR‑141 was detected by meRIP. The binding site between pri‑miR‑141 and METTL14 was determined by RIP. Results: We successfully upregulated METTL14 expression in MRC‑5 cells. Elevated METTL14 promoted MRC‑5 cell proliferation, suppressed its apoptosis and promoted inflammatory factors secretion in MRC‑5 cells. pri‑miR‑141 had m6A modification sites. pri‑miR‑141 can directly bind to METTL14. METTL14 upregulation increased miR‑141 while suppressed ZEB1 expression. Conclusion: METTL14 can promote the expression of miR‑141 by increasing the m6A modification site of pri‑miR‑141, and inhibit ZEB1, thereby promoting the proliferation of fibroblasts and the secretion of inflammatory factors.
