1.Surgical treatment and prognosis of 51 cases of splenic marginal lymphoma
Xinrong QU ; Zuyin LI ; Delin MA ; Runze ZHU ; Jie GAO
Chinese Journal of General Surgery 2023;38(8):600-604
Objective:To explore the clinical characteristics, treatment and prognosis of splenic marginal zone lymphoma.Methods:The clinical data of 51 patients with splenic marginal zone lymphoma who underwent surgical treatment at Department of Hepatobiliary in Peking University People's Hosipital from Dec 2009 to Oct 2022 were retrospectively analyzed.Results:The patients 's average age was 60.5±11.8 years old, and the ratio of male to female rate was about 1:1. As of the last follow-up date of Feb 28, 2023, 8 patients died of the primary lymphoma and 14 patients suffered from disease progression. The 5-year progression free survival rate was 68%, and the overall survival rate was 79%. Univariate analysis showed that age ≥65 years old, decreased preoperative albumin, increased bilirubin level, and increased lactate dehydrogenase bode ill for overall survival time, but none of them were independent risk factors; Age ≥65 years old and diffuse large B cell transformation were independent risk factors.Conclusions:Surgery combined with comprehensive treatment which contained rituximab is currently the main treatment method. Splenectomy remains an important treatment and diagnostic method for patients with obvious symptoms or persistent unrelieved blood count abnormalities and unexplained splenomegaly. Advanced age, elevated bilirubin and lactate dehydrogenase, decreased albumin, and diffuse large B cell transformation, it may indicate poor prognosis.
2.Mesenchymal stem cells inhibit hypoxic damage to rat pulmonary microvascular endothelial cells by regulating oxidative stress
Zhuang MAO ; Xue LI ; Changyao WANG ; Lin LYU ; Hu CAO ; Zhichao HE ; Zuyin YU ; Hua WANG
Chinese Journal of Pharmacology and Toxicology 2024;38(7):504-510
OBJECTIVE To explore the role and mechanism of dental pulp stem cells(DPSCs)in repairing hypoxic injury to rats pulmonary microvascular endothelial cells(PMVECs).METHODS ①PMVECs were treated with cobalt chloride at 0,10,25,50 and 100 μmol·L-1 for 72 h.CCK-8 was used to detect the cell viability,and the protein levels of hypoxia-inducible factor 1α(HIF-1α),zona occludens small-band protein 1(ZO-1),and occludin(OCLN)were detected by Western blotting.②There was a cell control group,model group,and model+DPSCs group,and the levels of reactive oxygen species(ROS)was detected by immunofluorescence staining after at 24 and 48 h of action.The levels of ZO-1 and OCLN proteins were detected by Western blotting.③ A cell control group,model group,model+DPSC group and model+DPSC cell knockdown superoxide dismutase 1(SOD1)group were set up.The mRNA level of SOD1 was detected by real-time fluorescence quantitative PCR 24 and 48 h later,while the protein levels of ZO-1 and OCLN were detected by Western blotting.RESULTS ① Com-pared with the cell control group,72 h of cobalt chloride 100 μmol·L-1 treatment of PMVECs resulted in a cell survival rate above 80%,a significant increase in the level of HIF-1α protein(P<0.05),a signifi-cant decrease in the levels of ZO-1 and OCLN proteins(P<0.01),and establishment of a model of hypoxic injury in PMVECs.② Compared with the cell control group,the ROS level was significantly higher in the model group(P<0.01).Compared with the model group,the ROS level was significantly lower in the model+DPSCs group(P<0.01),while the levels of ZO-1 and OCLN proteins were signifi-cantly higher in the model+DPSCs group(P<0.05).③ Compared with the DPSC group,ZO-1 and OCLN expressions were significantly decreased after knockdown of SOD1 in DPSCs(P<0.05,P<0.01).CONCLUSIONS DPSCs can repair hypoxic injury to PMVECs,and the anti-oxidative stress capacity of DPSCs plays an important role in hypoxic injury repair of PMVECs.
3.Cyclooxygenase-2 expressing hepatocellular carcinoma inhibits the infiltration and immune response of conventional type 1 dendritic cells
Yuzi LI ; Yang WANG ; Qian CHENG ; Zuyin LI ; Zhao LI ; Jiye ZHU ; Jie GAO
Chinese Journal of General Surgery 2024;39(5):372-378
Objective:To investigate the influence of COX-2 expression in hepatocellular carcinoma (HCC) on the infiltration and immune response of conventional type 1 dendritic cells (cDC1).Methods:Clinicopathological data from 111 HCC patients undergoing radical hepatectomy at Peking University People's Hospital from Jan 2016 to Jun 2017 were retrospectively analyzed. Immunofluorescence staining was employed to evaluate the cDC1 infiltration and COX-2 expression in tumor tissues. Patients were divided into two groups based on cDC1 infiltration: cDC1 enrichment and cDC1 depletion, and the correlation between COX-2 expression and cDC1 infiltration was analyzed. Single-cell sequencing of HCC tumor tissues was used to further investigate the correlation between PTGS2, the encoding gene of COX-2, and cDC1 infiltration. Hematopoietic stem cells (HSC) were utilized for in vitro generation of cDC1. HSC-derived cDC1s were sorted by FACS and cocultured with HCC cell line SNU423. Celecoxib, a selective COX-2 inhibitor, was used to suppress the COX-2 expression in HCC cell line SNU423. The functions of cDC1 were explored by FITC-dextran uptake assay, flow cytometry, and Luminex multiplex cytokine assay. Results:COX-2 expression was significantly higher in the cDC1 depletion group ( n=73) compared to the cDC1 enrichment group ( n=38) ( P=0.004 2). Patients with higher PTGS2 expression had significantly lower proportion of cDC1. Increased cDC1 infiltration in the HCC tumor microenvironment correlated with improved patient overall survival rates ( P=0.037) and disease-free survival rates ( P=0.048). Results from FITC-dextran uptake assay, flow cytometry, and Luminex assay indicated that cDC1 co-cultured with HCC showed significantly reduced antigen uptake function, co-stimulatory molecule expression, and cytokine secretion, but partially abrogated with celecoxib treatment. Conclusions:The intratumoral infiltration of cDC1 is positively correlated with favorable prognosis in HCC patients. Elevated COX-2 expression in HCC impedes the intratumoral accumulation of cDC1 and compromises their immune response capabilities. COX-2 inhibitors hold promise for enhancing cDC1 function in HCC.