ObjectiveTo investigate the therapeutic effect of Shaoyao Gancaotang （SYGCT） on high-fat diet （HFD）-aggravated colitis induced by dextran sulfate sodium （DSS） in mice and decipher the potential mechanism. MethodsForty male C57BL/6J mice were fed an HFD for 14 days， followed by gavage of 2%DSS for 7 days for the modeling of HFD-aggravated colitis. The mice were randomly allocated into control， model （HFD-aggravated colitis）， low-dose （5.2 g·kg^-1） SYGCT， high-dose （10.4 g·kg^-1） SYGCT， and 5-aminosalicylic acid （5-ASA， positive control， 50 mg·kg^-1） groups. Body mass changes and disease activity index （DAI） scores were recorded. The colon length was measured. Pathological changes in the colon tissue were observed through hematoxylin-eosin （HE） staining. Transcriptomic analysis was performed to identify differentially expressed genes. Western blot was employed to quantify the protein levels of Occludin， Claudin3， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， and ferritin heavy chain 1 （FTH1）. ResultsCompared with the control group， the model group exhibited diarrhea， bloody stools， increased DAI scores （P<0.01）， colon shortening （P<0.01）， severe colonic pathological damage， and reduced expression of tight junction proteins Occludin and Claudin3 （P<0.05， P<0.01）. Transcriptomic analysis revealed that the differentially expressed genes between the high-dose SYGCT group and the model group were significantly enriched in the ferroptosis signaling pathway. Compared with the model group， SYGCT treatment alleviated diarrhea and bloody stools， reduced DAI scores （P<0.01）， increased the colon length （P<0.01）， mitigated colonic pathological damage， and upregulated the expression of Occludin and Claudin3 （P<0.01）， as well as proteins （SLC7A11， GPX4， and FTH1） associated with the inhibition of ferroptosis （P<0.05）. ConclusionSYGCT significantly ameliorates HFD-aggravated DSS-induced colitis by suppressing ferroptosis via activation of the SLC7A11/GPX4 pathway.

Objective To observe the effects of Qingdu Decoction on intestinal barrier function by regulating the miR-34c-mediated signaling pathway of human mast cells-derived exosomes;To explore its molecular mechanism in the treatment of acute-on-chronic liver failure(ACLF).Methods An inflammatory model was established by treating human mast cells with 1 μg/mL lipopolysaccharide.The mast cells were over-expressed with miR-34c using lentiviral transfection,and were divided into normal group,model group and miR-34c over-expression group.Exosomes were extracted from each group of mast cells.Human intestinal epithelial cells were divided into normal group,normal exosome group,model exosome group,miR-34c over-expression exosome group and Qingdu Decoction group(miR-34c overexpression exosomes+Qingdu Decoction),and corresponding treatment was given.The dual luciferase gene report confirmed the targeting relationship between miR-34c and myeloma associated oncogene zinc finger protein(MAZ).RT-qPCR was used to detect the expression of miR-34c in mast cells and intestinal epithelial cells,and Western blot was used to detect the expressions of MAZ,Occludin and ZO-1 protein.Results Compared with the normal group,the expression of miR-34c in mast cells treated with lipopolysaccharide and transfected with lentivirus significantly increased(P<0.01).The results of the dual luciferase reporter gene experiment showed that miR-34c could target and inhibit MAZ expression.The RT-qPCR results showed that compared with the normal group,the miR-34c expression in intestinal epithelial cells significantly increased in the model exosome group and miR-34c over-expression exosome group(P<0.05,P<0.01),while the miR-34c expression in Qingdu Decoction group significantly decreased compared with the miR-34c over-expression exosome group(P<0.01).The Western blot results showed that compared with the normal group,the expressions of MAZ,Occludin and ZO-1 proteins in the model exosome group and miR-34c over-expressing exosome group were significantly reduced(P<0.05,P<0.01),while the expressions of MAZ,Occludin and ZO-1 proteins in Qingdu Decoction group significantly increased compared with the miR-34c over-expressing exosome group(P<0.05).Conclusion The treatment of ACLF with Qingdu Decoction may be related to the regulation of the miR-34c-mediated signaling pathway in mast cell-derived exosomes and the up-regulation of intestinal epithelial tight junction protein expression.

In traditional Chinese medicine,jaundice is a liver and gallbladder disorder,primarily characterized by yellowing of the eyes,skin,and urine,with ocular yellowing being the most prominent feature.The understanding of jaundice pathogenesis in traditional Chinese medicine can be traced back to the Inner Canon of Huangdi.Despite the continuous development and improvement of successive generations of medical practitioners and a rich theoretical understanding of its pathogenesis being formed by the end of the Qing Dynasty,no unified view exists on whether the core pathological factor was dampness or blood stasis,nor on whether the primary disease location lay in the spleen and stomach or the liver and gallbladder.This article re-examines historical perspectives on jaundice pathogenesis within the context of traditional Chinese medicine theory,focusing on two key issues:pathological factors and the location of Zang and Fu.By integrating modern research approaches based on compound pathogenesis theory,and considering pathological factors,disease location according to Zang and Fu,and disease progression,a theoretical model is reconstructed,centered on the intermingling of dampness and blood stasis and integration of liver and spleen.Additionally,the insights and therapeutic strategies of multiple renowned clinical hepatology experts are incorporated to enrich the theoretical framework for jaundice treatment in traditional Chinese medicine and to enhance clinical efficacy.

In traditional Chinese medicine,jaundice is a liver and gallbladder disorder,primarily characterized by yellowing of the eyes,skin,and urine,with ocular yellowing being the most prominent feature.The understanding of jaundice pathogenesis in traditional Chinese medicine can be traced back to the Inner Canon of Huangdi.Despite the continuous development and improvement of successive generations of medical practitioners and a rich theoretical understanding of its pathogenesis being formed by the end of the Qing Dynasty,no unified view exists on whether the core pathological factor was dampness or blood stasis,nor on whether the primary disease location lay in the spleen and stomach or the liver and gallbladder.This article re-examines historical perspectives on jaundice pathogenesis within the context of traditional Chinese medicine theory,focusing on two key issues:pathological factors and the location of Zang and Fu.By integrating modern research approaches based on compound pathogenesis theory,and considering pathological factors,disease location according to Zang and Fu,and disease progression,a theoretical model is reconstructed,centered on the intermingling of dampness and blood stasis and integration of liver and spleen.Additionally,the insights and therapeutic strategies of multiple renowned clinical hepatology experts are incorporated to enrich the theoretical framework for jaundice treatment in traditional Chinese medicine and to enhance clinical efficacy.

Objective To observe the effects of Qingdu Decoction on intestinal barrier function by regulating the miR-34c-mediated signaling pathway of human mast cells-derived exosomes;To explore its molecular mechanism in the treatment of acute-on-chronic liver failure(ACLF).Methods An inflammatory model was established by treating human mast cells with 1 μg/mL lipopolysaccharide.The mast cells were over-expressed with miR-34c using lentiviral transfection,and were divided into normal group,model group and miR-34c over-expression group.Exosomes were extracted from each group of mast cells.Human intestinal epithelial cells were divided into normal group,normal exosome group,model exosome group,miR-34c over-expression exosome group and Qingdu Decoction group(miR-34c overexpression exosomes+Qingdu Decoction),and corresponding treatment was given.The dual luciferase gene report confirmed the targeting relationship between miR-34c and myeloma associated oncogene zinc finger protein(MAZ).RT-qPCR was used to detect the expression of miR-34c in mast cells and intestinal epithelial cells,and Western blot was used to detect the expressions of MAZ,Occludin and ZO-1 protein.Results Compared with the normal group,the expression of miR-34c in mast cells treated with lipopolysaccharide and transfected with lentivirus significantly increased(P<0.01).The results of the dual luciferase reporter gene experiment showed that miR-34c could target and inhibit MAZ expression.The RT-qPCR results showed that compared with the normal group,the miR-34c expression in intestinal epithelial cells significantly increased in the model exosome group and miR-34c over-expression exosome group(P<0.05,P<0.01),while the miR-34c expression in Qingdu Decoction group significantly decreased compared with the miR-34c over-expression exosome group(P<0.01).The Western blot results showed that compared with the normal group,the expressions of MAZ,Occludin and ZO-1 proteins in the model exosome group and miR-34c over-expressing exosome group were significantly reduced(P<0.05,P<0.01),while the expressions of MAZ,Occludin and ZO-1 proteins in Qingdu Decoction group significantly increased compared with the miR-34c over-expressing exosome group(P<0.05).Conclusion The treatment of ACLF with Qingdu Decoction may be related to the regulation of the miR-34c-mediated signaling pathway in mast cell-derived exosomes and the up-regulation of intestinal epithelial tight junction protein expression.

ObjectiveTo dynamically observe the effects ofJieduan Niwan Formula on mitochondrial apoptotic pathway in acute-on-chronic liver failure (ACLF) rats; To further reveal the possible mechanism ofJieduan Niwan Formula.MethodsSPF Wistar rats were randomly divided into normal group, model group andJieduan Niwan group. 13-week porcine serum injection followed withD-galactosamine and lipopolysaccharide joint acute attack was used to established ACLF model in all rats except for normal group. Rats inJieduan Niwangroup were orally givenJieduan NiwanFormula for 3 days before acute attack. Rats were sacrificed respectively at 4, 8 and 12 h after models were established. The expressions of Bid, Cytochrome C (Cyt C) and hepatocyte ultrastructure were detected by Western blot method, immunohistochemical analysis and transmission electron microscope, respectively.Results Compared with normal group, the levels of Cyt C and Bid in model group increased at 4 h and peaked at 8 h but decreased at 12 h (P<0.05); however, the levels of Cyt C and Bid inJieduan Niwan group were lower than those in model group at 4 and 8 h but higher at 12 h (P<0.05). The ultrastructures were significantly damaged in model rats, which severity was escalated through time; inJieduan Niwan group, the degree of injury decreased at each timing.ConclusionJieduan NiwanFormula can efficiently alleviate the hepatocyte damage in ACLF rats, and the mechanism might be involved in the inhibition of the mitochondrial apoptotic pathway.

Objective To evaluate the effect of psychological interventions for patients with urnary cancer on pain and quality of life.Methods One hundred and twenty patients were randomized into research and control group.Each group contained 60 cases. The study group received regular analgesic treatment and psychological interventions.The control group received the same scheme but for psychological interventions.As LQ-C30 was applied to evaluate patients' pain intensity and quality of life respectively.Result The pain relief rate of study group acquired is different significantly from control group, as well as in a higher score in global quality of life, role function, emotional function (P<0.05).Conclusions High-quality psychological care service can improve the quality of life of patients and release cancer pain.

Chronic ulcer of the lower extremities amounts for a grave and serious problem for public health. Western medicine focuses on controlling infection, improving blood circulation, surgical debridement, skin grafting, etc, but there are bottlenecks in the treatment. Traditional Chinese medicine (TCM) has a long history and a legacy of sound clinical efficacy in this area. TCM has developed a unique, effective external theory, and a large number of topical prescriptions and external technology. Through this research, a safe and effective treatment protocol of TCM for chronic ulcer of the lower extremities can be formed. To this end, during China's "Eleventh Five-Year" Plan, special research committees and projects on TCM external treatments and external technologies were established. This study on ulcer of the lower extremities constitutes one of the major research topics.

Objective To study the therapeutic effect and mechanism of Jiawei Xiaochengqi Decoction on hepatic injures by endotoxin in rats. Methods Endotoxemia model of Wistar rats was made by thioacetamide. Blood biochemistry and pathological changes were examined to observe the effect of Jiawei Xiaochengqi decoction on liver function, TNF-?, endotoxin of the model rats. Results Jiawei Xiaochengqi Decoction could reduce the contents of TNF-?, endotoxin in the blood and the degree of hepatic cells necrosis of Wistar rats. There was significant difference compared with model group (P