This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). In vitro, norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.
OBJECTIVE: To investigate the diagnostic criteria and therapeutic method of the Klippel-Trenaunay syndrome. METHODS: Among 5 cases, there were 2 males and 3 females aged from 11 days to 73 years. Vasography was carried out in all five patients and MRA was performed in one patients. RESULTS: After operation, the symptoms improved in 4 cases: the portine-like erythemas on their limbs got unclear; the focuses diminished obviously; the circumferences of the suffered limbs shrank and the ulcer healed. For following-up period was not long enough, the long term therapeatic result was still uncertain. CONCLUSION: Once the diagnosis of the Klippel-Trenaunay syndrome was made, operation should be performed as early as possible. If the surgical time is selected in prepuberty, optimal result can be expected.
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.
【摘要】 目的 研究肥大細胞膜穩定劑色甘酸二鈉（disordium cromoglycate，DC）對葡聚糖硫酸鈉（dextran sulfate sodium，DSS）誘導的大鼠急性結腸炎的影響。 方法 出生80~100 d的雄性SD清潔級大鼠30只，體重180~250 g。30只大鼠隨機分為3組:正常對照組（A組）、潰瘍性結腸炎組（B組）和DC組（C組），每組各10只。B組和C組自由飲用40 g/L DSS溶液（4%） 7 d誘發急性結腸炎，同時C組每天按100 mg/kg腹腔注射DC 1次，A組和B組每天腹腔注射等量的生理鹽水。7 d后，處死各組大鼠。對各組大鼠行疾病活動指數評分，結腸組織行大體評分、組織學評分，檢測門靜脈血一氧化氮濃度，結腸組織髓過氧化物酶活性。 結果 疾病活動指數評分、大體評分、組織學評分、一氧化氮濃度及髓過氧化物酶活性均表現為B組gt;C組gt;A組（Plt;0.05）。 結論 肥大細胞膜穩定劑DC對DSS誘導的大鼠急性結腸炎有一定的保護作用。【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.