抗菌消炎合剂的药理研究

抗菌消炎合剂对巴豆油所致小鼠耳肿胀和角叉菜胶所致大鼠中肿胀有明显的抑制作用，并能明显地抗二甲苯引起的小鼠皮肤毛细血管通透性增加。体外抗菌试验显示本药对金黄色葡萄球菌，卡他球菌和肺炎链球菌等有抑菌作用。     

Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes

Pancreatic islet beta-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. beta-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes beta-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to beta-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block beta-cell apoptosis could be a significant new development in type 1 and 2 diabetes.     

Involvement of hydrogen peroxide in the differentiation and apoptosis of preosteoclastic cells exposed to arsenite

Long-term exposure to sodium arsenite (AsO₂) promotes the development of various cancers. Paradoxically, arsenic also induces pro-myelomonocytic leukemia cell differentiation, and at higher concentrations, apoptosis. The present study investigated the effects of AsO₂ on preosteoclasts. When treated with 2.5-5 μM AsO₂, RAW264.7 cells underwent osteoclast differentiation as evidenced by an increase in the number of multinucleate cells expressing tartrate resistant acid phosphatase (TRAP). The appearance of these phenotypic markers was preceded by a low level increase in extracellular production of H₂O₂ and was prevented by the addition of catalase (4.5 μg/ml), an enzyme that removes H₂O₂. Only at high concentrations (10-25 μM) of AsO₂ was a significant loss of cell viability and a high level increase in H₂O₂ production (1.5 μM) observed. Apoptosis was blocked by pretreatment with diphenylene iodonium chloride (2 μM), a NAD(P)H-flavoprotein inhibitor, suggesting the involvement of NADPH-oxidase. The data show that AsO₂, dose-dependently, stimulates increasing amounts of H₂O₂ production. Moreover, at concentrations found in tissues of individuals exposed to geochemical AsO₂, osteoclasts underwent an H₂O₂-dependent differentiation. Therefore, chronic exposure to low-level amounts of AsO₂ could result in increased bone resorption and contribute to bone related pathologies.     

S100A8 and S100A9 in inflammation and cancer

Calprotectin (S100A8/A9), a heterodimer of the two calcium-binding proteins S100A8 and S100A9, was originally discovered as immunogenic protein expressed and secreted by neutrophils. Subsequently, it has emerged as important pro-inflammatory mediator in acute and chronic inflammation. More recently, increased S100A8 and S100A9 levels were also detected in various human cancers, presenting abundant expression in neoplastic tumor cells as well as infiltrating immune cells. Although, many possible functions have been proposed for S100A8/A9, its biological role still remains to be defined. Altogether, its expression and potential cytokine-like function in inflammation and in cancer suggests that S100A8/A9 may play a key role in inflammation-associated cancer.     

Involvement of multiple signaling pathways in the post-bariatric induction of IL-6 and IL-8 mRNA and release in human visceral adipose tissue

The present studies were designed to determine the site of and the mechanism for the rapid increase in IL-6 and IL-8 mRNA observed in human visceral adipose tissue after removal during laparoscopic bariatric surgery. Upregulation of IL-6 and IL-8 mRNA as well as their release were seen within 3h whether one intact piece of tissue or minced pieces of adipose tissue were incubated in vitro. Most of the IL-6 and IL-8 mRNA content of visceral adipose tissue after 3h of incubation was in the non-fat cells. Actinomcyin D markedly reduced the upregulation of IL-6 and IL-8 mRNA. Incubation of adipose tissue explants with a soluble TNFalpha receptor (etanercept) plus a blocking antibody against IL-lbeta reduced by 55% the increase in IL-6 mRNA and by 42% that of IL-8 mRNA seen between 1 and 5h of incubation. The upregulation of IL-8 and IL-6 mRNA accumulation as well as their release over a 2 or 4h incubation was reduced by around 50% in the presence of an inhibitor of the p38 MAPK or an inhibitor of the NFkappaB pathway and by 85% in the presence of both inhibitors. The data suggest that the relative trauma and/or hypoxia that occurs when adipose tissue is removed results in the release of TNFalpha and IL-1beta. These cytokines, and probably other factors as well, enhance IL-6 and IL-8 mRNA accumulation in human adipose tissue explants through mechanisms involving the p38 MAPK and NFkappaB pathways.     

加味补阳还五汤对周围神经损伤后神经机能恢复的实验研究

用加味补阳还五汤制剂给大鼠腓总神经损伤后的动物模型灌胃治疗,以观察该药物对周围神经损伤后神经机能恢复的作用。研究结果显示:用药组各观察周期运动神经传导速度均快于对照组(p<0.001);损伤后神经纤维传导速度的恢复率和伤肢的功能恢复用药组亦快于和早于对照组。     

杨之藻主任医师治疗小儿紫癜肾经验

杨之藻主任医师认为，小儿紫癜肾初期以实证为主，后期多为虚实互见。实证治法强调疏风清热和活血化瘀，坚持辨证论治，倡导中西医结舍。对过敏原的检测、过敏性紫癜病人的饮食安排等问题提出了自己的看法。     

电针督脉和足太阳经穴对抑郁症大鼠模型海马神经元的影响

目的:观察电针督脉经穴("百会"、"神庭")的基础上加用足太阳经穴("心俞"、"肝俞")对抑郁症大鼠体重和海马神经元损伤的影响。方法:采用长期不可预见性中等强度应激结合孤养造成大鼠抑郁症模型,运用免疫荧光技术观察电针对抑郁大鼠体重和海马神经元损伤的影响。结果:电针督脉加足太阳经穴可使抑郁症大鼠的体重增加迟缓,使抑郁大鼠海马CA1、CA3区及齿状回(DG)神经元数目显著增加。结论:电针督脉加足太阳经穴可能通过减轻大鼠海马神经元的损伤,从而改善动物的抑郁病情。