ABSTRACT
Intracranial aneurysm is a common cerebrovascular disease, which has a high morbidity and mortality after rupture, usually resulting in poor prognosis. Intracranial aneurysms are mainly treated by craniotomy clipping and endovascular embolization, but there is still controversy about whether the unruptured aneurysms with a diameter of <5 mm need intervention. Studies have shown that inflammation plays an important role in the formation, progression, and rupture of intracranial aneurysms. Aspirin and statins can delay the development of intracranial aneurysms and help reduce the risk of rupture through anti-inflammatory. This article reviews the inflammatory mechanism and potential drug therapy of intracranial aneurysms.
ABSTRACT
Mycoplasma pneumoniae(MP)infection and asthma are common respiratory diseases in children, and they are closely related.MP infection induces asthma attacks, and anti-MP infection treatment can help control the degree in children with asthma.This article describes the relationship between MP infection and asthma, and provides a theoretical basis for the treatment of asthma.MP infection can damage the airway and cause chronic cough and bronchial asthma attacks.MP infects the airway epithelium and secretes community-acquired respiratory distress syndrome toxin(CARDS Tx)combined with the airway mucosa to cause the airway epithelial damage, and promotes the body to form a TH2-mediated immune response, mediates the production of specific IgE, and then triggers the release of inflammatory mediators involved in asthma; the increase of inflammatory factors released after MP infection will also cause exhaled breath.Fractional exhaled nitric oxide(FeNO)is elevated, which can lead to airway hyperresponsiveness and airway remodeling.In view of treatment, when treating MP infections with macrolide drugs, they can also have anti-inflammatory and immunomodulatory effects on the airways, which can reduce the steroid dose required by children with steroid-dependent asthma, reduce the frequency of asthma attacks and prolong remission period in children with asthma.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of tumor necrosis factor-α (TNF-α) on nutritional status and proteolysis of respiratory muscle in a rat model of chronic obstructive pulmonary disease (COPD).</p><p><b>METHODS</b>Ninety healthy male adult Wistar rats were randomly divided into model group (A) and normal control group (B). COPD malnutrition rat models were established by cigarettes smoke and nutrient limitation and divided into normal nutrition COPD group (A(1)), malnutrition COPD group (A(2)), and malnutrition COPD intervention group (A(3)). In group A(3), the rats received intravenous injection of TNF-α mAb (0.1 mg/kg). TNF-α levels in the serum and respiratory muscle homogenates were measured using enzyme-linked immunosorbent assay (ELISA), and plasma levels of glucose, albumin, and triglyceride were measured with an automatic biochemistry analyzer. High-performance liquid chromatography was used to measure the contents of 3-methylhistidine and tyrosine in the respiratory muscle homogenates.</p><p><b>RESULTS</b>The serum TNF-α level and plasma levels of glucose and triglyceride were significantly higher but the plasma albumin level was significantly lower in group A(2) than in groups B, A(1), and A(3) (P<0.01). The contents of 3-MH and Tyr in the respiratory muscle homogenates were significantly higher in group A(2) than in the other 3 groups (P<0.01, P<0.01). TNF-α in the respiratory muscle showed a strong positive correlation to 3-MH and Tyr.</p><p><b>CONCLUSION</b>TNF-α is one of the causes of increased proteolysis of the respiratory muscle.</p>
Subject(s)
Animals , Male , Rats , Lung , Pathology , Nutritional Status , Proteolysis , Pulmonary Disease, Chronic Obstructive , Metabolism , Pathology , Respiratory Muscles , Metabolism , Tobacco Products , Tumor Necrosis Factor-alpha , PharmacologyABSTRACT
OBJECTIVE@#To explore the effect of different concentrations of vitamin C on proliferation and apoptosis of C(2)C(12) myoblasts.@*METHODS@#C(2)C(12) cells cultured in vitro were collected by trypsinization to form monoplast suspension, and then centrifuged to float again. The cellular numbers were counted and the cell suspension density adjusted, and the cells were inoculated into 96-shadow mask according to 200 μL per hollow. All cells were cultured in the normal way. While cell fusion ratio arrived 80% and cells did not differentiate, cells were divided into 6 groups: a negative control group (pure DMEM-F12 medium), an H(2)O(2) group (DMEM-F12 medium containing 500 μmol/L H(2)O(2)) and vitamin C group 1 to 4(DMEM-F12 medium containing 500 μmol/L H(2)O(2) and 10, 20, 60, and 100 mg/L vitamin C, respectively). After each group was treated for 0, 6, 24, 36, 48,and 72 h, respectively, MTT was used to detect C(2)C(12) cell proliferation in each group. Annexin V-PI double staining was applied to detect C(2)C(12) cell apoptosis in each group after treatment for 36 h.@*RESULTS@#After the cells were treated for 36 h and 72 h, the absorbance of vitamin C group 1 to 4 were higher than that of H(2)O(2) group (P<0.001). The absorbance of vitamin C group 4 was the highest among all the groups, significantly higher than that of the negative control group when the cells were treated for 36 h (P<0.05). When the cells were treated for 36 h, the C(2)C(12) cells apoptosis rate of vitamin C group 2 to 4 was lower than that of H(2)O(2) group; The C(2)C(12) cells apoptosis rate of vitamin C group 2 and 3 was higher than that of the negative control group, while the C(2)C(12) cells apoptosis rate of vitamin C group 4 was significantly lower than that of the negative control group (P=0.009).@*CONCLUSION@#Vitamin C can efficiently inhibit the apoptosis of C(2)C(12) myoblasts induced by H(2)O(2), and after 36 h intervention, high concentration vitamin C may promote C(2)C(12) the proliferation of myoblasts.