ObjectiveTo investigate the possible mechanism affecting liver cirrhosis by splenectomy. MethodsBy subcutaneous administration of 20% carbon tetrachloride(CCl4), liver cirrhosis models were established in splenectomy and nonsplenectomy groups. After HE staining, special staining and immunohistochemical staining, mast cell, Kupffer’s cell and Ito cell were counted under optical microscope. Liver pathological sections and the dynamic changes of these cells in mice were studied respectively in comparison with the normal group.ResultsThe incidence of liver cirrhosis in nonsplenectomy group was significantly higher than that in splenectomy group after the 16th injection of CCl4 (P＜0.05). The count of mast cell was much higher than that in splenectomy group after the 4th and the 8th injection (P＜0.05). Kupffer’s cell and Ito cell significantly increased after the 12th and the 16th injection in nonsplenectomy group compared with splenectomy group (P＜0.05). ConclusionSplenectomy may decline the incidence of hepatic cirrhosis caused by multifactors. In the early stage, splenectomy influences the migration, maturation and accumulation of mast cell. In the middle and late stage, it influences the proliferation of Kupper’s cell and cytokine secretion, thus the Ito cells are activated and proliferation is inhibited, in which extracellular matrix decreases in amount and the degree of hepatic fibrosis is reduced.
【摘要】 目的 研究肥大细胞膜稳定剂色甘酸二钠（disordium cromoglycate，DC）对葡聚糖硫酸钠（dextran sulfate sodium，DSS）诱导的大鼠急性结肠炎的影响。 方法 出生80~100 d的雄性SD清洁级大鼠30只，体重180~250 g。30只大鼠随机分为3组:正常对照组（A组）、溃疡性结肠炎组（B组）和DC组（C组），每组各10只。B组和C组自由饮用40 g/L DSS溶液（4%） 7 d诱发急性结肠炎，同时C组每天按100 mg/kg腹腔注射DC 1次，A组和B组每天腹腔注射等量的生理盐水。7 d后，处死各组大鼠。对各组大鼠行疾病活动指数评分，结肠组织行大体评分、组织学评分，检测门静脉血一氧化氮浓度，结肠组织髓过氧化物酶活性。 结果 疾病活动指数评分、大体评分、组织学评分、一氧化氮浓度及髓过氧化物酶活性均表现为B组gt;C组gt;A组（Plt;0.05）。 结论 肥大细胞膜稳定剂DC对DSS诱导的大鼠急性结肠炎有一定的保护作用。【Abstract】 Objective To observe the influence of the mast cell memebrane stabilizer, disordium cromoglycate (DC), on dextran sulfate sodium (DSS)-induced colitis in rats. Methods Thirty male Sprague-Dawley (SD) rats aged 80 to 100 days with their weight ranged from 180 to 250 g were randomly divided into 3 groups: normal control group (group A), dextran sulfate sodium group (group B) and disordium cromoglycate group (group C), with 10 rats in each. Rats in group B and C drank 40 g/L DSS solution (4%) for 7 days to induce acute colitis. At the same time, intraperitoneal administration of DC (100 mg/kg) to rats in group C was carried out once a day, while the other two groups of rats were given the same amount of normal saline solution. Disease activity index (DAI), gross and histological evaluation were analyzed. NO concentration of blood from portal vein was measured. Myeloperoxidase (MPO) activity of colonic tissue was detected. Results The experimental data of group C, including DAI, gross evaluation, histological assessment, NO concentration and MPO activity, were all significantly higher than those of group A (Plt;0.05), but lower than those of group B (Plt;0.05). Conclusion Disordium cromoglycate can protect the colon of rats with DSS-induced acute colitis.
【Abstract】Objective To investigate the expression of extracellular matrix metalloproteinase inducer(EMMPRIN)，matrix metalloproteinase-1(MMP1)，MMP9，tissue inhibitors of metalloproteinase-1(TIMP1) and the mast cell count (MCC) and to detect their clinicopathologic significance and relationship in pancreatic cancer tissues. Methods Immunohistochemical method of avidin-biotin complex was used for those 5 targets on the routinely paraffinembedded sections of surgical resected specimen of 51 cases with pancreatic carcinoma. Results The positive rates of EMMPRIN，MMP1，MMP9 and TIMP1 were 56.9%，54.9%，60.8% and 49.0% and its scoring were 2.5±1.5，2.3±1.9，2.4±1.6 and 1.9±1.6 respectively. The mean of MCC was (16.1±6.8)/HP in total cases. The positive rates or scorings of EMMPRIN，MMP1，MMP9 and MCC were significantly lower in high differentiated or without-metastatic cases than in low differentiated or with-metastatic ones(P＜0.05 or P＜0.01), and those targets (except MCC and scoring of MMP9) of middle differentiated ones were lower than those of low differentiated while that of TIMP1 was opposite(P＜0.01). The MCC showed significantly higher in the positive cases of EMMPRIN, MMP1 and MMP9 or negative cases of TIMP1 than in the negative ones of EMMPRIN, MMP1 and MMP9 or positive ones of TIMP1. The closely positive correlations were found among the MCC and the scoring of EMMPRIN, MMP1 and MMP9. The closely negative correlations existed among the scoring of TIMP1 and the other four targets.Conclusion The MCC and the expressions of EMMPRIN, MMP1, MMP9 and TIMP1 might be important biological markers for reflecting the progression and the prognosis of pancreatic carcinoma. They might have co-regulated effects on the potentials of invasion and metastasis of pancreatic carcinoma or other malignant lesions.
Objective To investigate the effect of tranilast on wound healing and the mechanism of inhibiting scar hyperplasia in mice, and to study the relationship between the inhibiting ability of tranilast on scar hyperplasia and administration time. Methods Sixty-six Kunming mice were selected to build deep II degree burn model, and were randomly divided into the control group (18 mice), the early intervention group (18 mice), the medium intervention group (18 mice), and the late intervention group (12 mice). The mice in the early intervention group, the medium-term intervention group, and the late intervention group were given tranilast 200 mg/(kg·d) by gastrogavage at immediate, 7 days, and 14 days after burn respectively, and the mice in the control group were managed with same amount of normal saline every day. The wound healing was observed regularly. At 14, 28, and 42 days in the early and medium intervention groups and at 28 and 42 days in the late intervention group, fresh tissues were taken from 6 mice to observe the shape of mast cells by toluidine blue staining, collagen content by Masson staining; the collagen type I and collagen type III content were measured to calculate the I/III collagen content ratio by immunohistochemistry method, the contents of transforming growth factor β1 (TGF-β1) and histamine were detected by ELISA; and the ultrastructure of fibroblasts was observed under transmission electron microscope. Results There was no significant difference in wound healing time between groups (F=1.105,P=0.371). The mast cells number, collagen content, TGF-β1 content, histamine content, and the I/III collagen content ratio in the early intervention group were significantly less than those in the other groups (P<0.05). Significant difference was found in mast cells number, collagen content, and histamine content between control group and medium or late intervention group at the other time points (P<0.05) except between control group and late intervention group at 42 days (P>0.05). Compared with the control group, the activity of fibroblasts in the early intervention group was obviously inhibited, and the arrangement of the fibers was more regular; the fibroblast activity in the medium and late intervention groups was also inhibited obviously. Conclusion Tranilast has no obvious effect on the wound healing time in mice. Tranilast intervention shows the inhibitory effect on the scar hyperplasia which can significantly reduce the number of mast cells, the content of histamine and TGF-β1, inhibit the ability of fibroblasts synthetic collagen and adjust the proportion of collagen synthesis. The immediate tranilast intervention may have the best inhibitory effect on scar hyperplasia.
Deep hypothermic circulatory arrest (DHCA) is an important assistant technique for complex cardiac surgery, which creates convenient operating conditions for surgery, and is also one of the measures to protect the brain during operation. However, the complications caused by this technique cannot be ignored, and it should be noticed that the occurrence of intestinal injury is relatively insidious, but brings great pain to patients and significantly reduces the quality of life after operation. Studies have shown that intestinal ischemia-reperfusion injury is induced by DHCA. It causes mast cells to activate and release many inflammatory mediators that destroy the intestinal mucosal epithelium barrier, and eventually lead to intestinal injury. This article reviewed the research progress of mast cells in the mechanism of DHCA-induced intestinal injury.
Objective To investigate the relationship between the expression of mast cell expressed membrane protein 1 (MCEMP1) in gastric cancer and its relationship with prognosis and tumor immune infiltration. Methods Transcriptome expression profile data and clinical data information of gastric cancer and normal samples were downloaded from TCGA database, and differentially expressed genes in gastric cancer tumor microenvironment were extracted using R 4.0.5 software. Protein-protein interaction network of differentially expressed genes was constructed by using STRING online website, protein-protein interaction network and univariate Cox proportional hazards regression analysis were used for cross-tabulation analysis to obtain key genes. Kruskal-Wallis rank sum test was used to investigate the correlation between key genes and clinicopathological features. The possible signaling pathways involved in key genes were predicted by gene set enrichment analysis. We further analyzed the relationship between expression of key gene and the level of immune infiltration and immune molecules in gastric cancer by TISIDB online database and CIBERSORT algorithm. Results A total of 760 differentially expressed genes in gastric cancer were found and a key gene of MCEMP1 was derived from cross-tabulation analysis based on the results of protein-protein interaction network and univariate Cox proportional hazards regression analysis. Expression of MCEMP1 was significantly upregulated in gastric cancer tissues (P<0.001), and survival analysis showed that the overall survival rate of the group with high expression level of MCEMP1 was lower than that of low expression [HR=1.176, 95%CI (1.066, 1.297）, P=0.046]. Expression of MCEMP1 also correlated with age, T-stage, and clinical stage of gastric cancer (P<0.05) , and expression of MCEMP1 was significantly associated with a variety kinds of immune cells and expression of immune molecules (P<0.05). Conclusion MCEMP1 is a potential prognostic marker for gastric cancer and is associated with immune infiltration in gastric cancer.
Mast cell (MC) play a crucial role in non-allergic fundus diseases, including uveitis, diabetic retinopathy, and age-related macular degeneration. MCs can profoundly influence the pathological processes of these diseases by regulating inflammatory responses, promoting angiogenesis, and facilitating tissue remodeling through the degranulation and release of mediators such as histamine, cytokines, and enzymes. The application of MC-associated inhibitors has been shown to effectively mitigate or inhibit the progression of these pathologies, offering a promising strategy for treating ocular diseases. Understanding the current state of MC research in fundus diseases will enhance our insight into their role in the pathophysiological mechanisms of these conditions and encourage further research aimed at providing more effective treatment options for patients.