Methods: Inflammatory mediators including IL-1β, IL-6, IL-8, TNF-α,and LTB_4 were measured,which were released from polymorphonuclear (PMN) cells collected from normal subjects and pretreated by homoeriodictyol-7-O-β-D-glycoside with PAF stimulating.
This study has been designed to compare the contralateral lung injury by injecting HC1 and Pepsin to single lung of rabbits, and the patho-genesis was investigated by examining the changes in inflammatory mediators TXB2, 6K - PGF_(1a), in order to provide theoretical evidence for its treatment.
The result showed that the moxibustion alleviated the inflammatory reaction and significantly reduced the level of the chemical inflammatory mediator(Hm, 5-HT) and the inflammatory cytokine (TNF, IL-1β) (P < 0. 05 or P < 0. 01. comparing with control group).
Objective: To investigate the clinical therapeutic effect of Qingfeihuatan Quyu prescription(清肺化痰祛瘀方,苇茎汤加碱) on treatment of chronic obstructive pulmonary disease(COPD) in acute(deteriorated) stage and its intervention effect on inflammatory mediator in plasma.
This study was designed to observe the association of the polymorphisms of inflammatory medium interleukin 6 gene promoter region in circulation with interleukin 6,high sensitive C reactive protein and fibrinogen in circulation among the healthy population in Beijing city,and assess the race difference of the polymorphisms of interleukin 6 gene.
Results The PYKS obviously raised the expression of Caspase-3 and MMP-2, but decreased the expression of NF-κB. Conclusion The anti-inflammatory mechanism of the PYKS possibly raised the expression of Caspase-3 and MMP-2 of mice endometrial cells, decreased the expression of NF-κB, so as to reduce inflammation soakage in excess and formation of inflammatory medium, accelerate apoptosis and reduce local inflammation.
With the role of causative agent, the increase and interaction of various kinds of digestive enzymes and inflammation mediators such as cytokines, reactive oxygen species (ROS), endotoxin, NF-κB resulted in the injury of pancreas and distant organ.
Background and objectives: Bronchial asthma (abbreviating asthma) is a chronic disease that seriously threaten human health over the world, it is a kind of chronic inflammation of airway, which is induced by a series of inflammation mediators, such as mast cells, eosinophils , T lymphocytes and so on.
Upon stimulation by inflammatory mediators, the gelatinase granules are secreted before the common peroxidase-negative granules.
Either factor alone, be it respiratory virus infection or inflammatory mediators (chemokines, neutrophils, or reactive oxygen species), is insufficient to cause desquamation.
In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier.
Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis (SAP) in multiple organ injury is a hotspot in the surgical field.
Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR (oxygen free radical), endotoxin, etc.
Nitric oxide (NO) is a nonspecific inflammatory mediator that has been involved in the pathogenesis of multiple sclerosis (MS).
Among them, tumor necrosis factor (TNF)-α, a multipotent pro-inflammatory mediator, plays a critical role in immunoregulation of asthma by contributing to bronchopulmonary inflammation and airway hyperresponsiveness.
H4R is involved in chemotaxis and inflammatory mediator release by eosinophils, mast cells, monocytes, dendritic cells, and T cells.
The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS).
Reactions are often tissue- and cell-specific, and provide a spectrum of inflammatory mediator release in which many of the molecular details remain to be elucidated.