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.
【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.
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.