目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期...目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期等病理特征和预后的影响。方法组织标本来自于2012年3月至2015年2月我院接受手术治疗的78例DLBCL患者和30例反应增生性淋巴结患者,采用免疫组化方法比较DLBCL患者和反应增生性淋巴结患者淋巴组织NF-κB/p65、Bcl-2和Bax蛋白表达情况,分析它们与病理参数、生存期的关系。结果 DLBCL组织中,NF-κB/p65和Bcl-2阳性率分别为39.74%和51.28%,显著高于反应增生性淋巴结组织(P<0.05),Bax阳性率为32.05%,显著低于反应增生性淋巴结组织(P<0.05);DLBCL组织NF-κB/p65阳性表达与B症状、IPI得分、临床分期有关(P<0.05),Bcl-2阳性表达与IPI得分、临床分期有关(P<0.05),Bax阳性表达与临床分期有关(P<0.05);NF-κB/p65与Bcl-2呈正相关(r=0.53,P<0.05),NF-κB/p65与Bax呈负相关(r=-0.51,P<0.05),Bcl-2与Bax呈负相关(r=-0.62,P<0.05);NF-κB/p65、Bcl-2阳性表达者生存期较短,Bax阳性表达者生存期较长。结论DLBCL组织中NF-κB/p65、Bcl-2高表达,Bax低表达,有助于DLBCL预后评估。展开更多
Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-i...Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.展开更多
文摘目的探讨弥漫性大B细胞淋巴瘤(diffuse large B cell lymphoma,DLBCL)组织核转录因子κB(nuclear factor-kappa B,NF-κB)/p65、Bcl-2和Bax蛋白表达及其对临床B症状、国际预后指数(international prognostic index,IPI)得分、临床分期等病理特征和预后的影响。方法组织标本来自于2012年3月至2015年2月我院接受手术治疗的78例DLBCL患者和30例反应增生性淋巴结患者,采用免疫组化方法比较DLBCL患者和反应增生性淋巴结患者淋巴组织NF-κB/p65、Bcl-2和Bax蛋白表达情况,分析它们与病理参数、生存期的关系。结果 DLBCL组织中,NF-κB/p65和Bcl-2阳性率分别为39.74%和51.28%,显著高于反应增生性淋巴结组织(P<0.05),Bax阳性率为32.05%,显著低于反应增生性淋巴结组织(P<0.05);DLBCL组织NF-κB/p65阳性表达与B症状、IPI得分、临床分期有关(P<0.05),Bcl-2阳性表达与IPI得分、临床分期有关(P<0.05),Bax阳性表达与临床分期有关(P<0.05);NF-κB/p65与Bcl-2呈正相关(r=0.53,P<0.05),NF-κB/p65与Bax呈负相关(r=-0.51,P<0.05),Bcl-2与Bax呈负相关(r=-0.62,P<0.05);NF-κB/p65、Bcl-2阳性表达者生存期较短,Bax阳性表达者生存期较长。结论DLBCL组织中NF-κB/p65、Bcl-2高表达,Bax低表达,有助于DLBCL预后评估。
基金National Natural Science Foundation of China(grant numbers 82174143)the Innovative Team Project of Ordinary Universities in Guangdong Province(grant numbers 2022KCXTD016).
文摘Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.