Bronchopulmonary Dysplasia ; etiology ; pathology ; prevention & control ; Humans ; Infant, Newborn ; Infant, Premature ; Inflammation ; complications ; Lung ; pathology ; Respiration, Artificial ; adverse effects

The inflammation factors and roles of them in acute coronary syndrome (ACS) were explored. The similarity between the theory of pathogenic toxin in Chinese Medicine and the inflammation response theory in ACS was discussed. The exploration of new inflammatory factors may be helpful for Chinese Medicine in the research of ACS.
Acute Coronary Syndrome ; complications ; diagnosis ; prevention & control ; therapy ; Humans ; Inflammation ; complications ; etiology ; pathology ; therapy ; Inflammation Mediators ; physiology ; Medicine, Chinese Traditional ; Prognosis ; Toxins, Biological ; adverse effects

Atopic dermatitis (AD) is among the most common skin disorders in humans. Although a variety of regimens are available for the treatment of AD, preventive approaches are limited. Recent studies have demonstrated that certain naturally-occurring herbal medicines are effective in preventing the development of AD via divergent mechanisms, such as inhibiting cytokine and chemokine expression, IgE production, inflammatory cell infiltration, histamine release, and/or enhancement of epidermal permeability barrier function. Yet, they exhibit few adverse effects. Since herbal medicines are widely available, inexpensive and generally safe, they could represent an ideal approach for preventing the development of AD, in both highly developed and developing countries.
Animals ; Chemokines ; metabolism ; Dermatitis, Atopic ; prevention & control ; Disease Models, Animal ; Herbal Medicine ; Humans ; Immunoglobulin E ; metabolism ; Inflammation ; pathology

A visible cutaneous scar develops from the excess formation of immature collagen in response to an inflammatory reaction. This study examined the role of epidermal growth factor (EGF) in the formation of cutaneous scars. Twenty Crl:CD-1 (ICR) mice were used and 2 full-thickness skin wounds were made on the dorsum of each mouse. One of the wounds was treated with recombinant human EGF by local application and the other was treated with saline for control until complete healing was achieved. The EGF-treated group's wounds healed faster than the control group's. The width of the scar was smaller by 30% and the area was smaller by 26% in the EGF-treated group. Inflammatory cell numbers were significantly lower in the EGF-treated group. The expression of transforming growth factor (TGF)-beta1 in the EGF-treated group was increased. It was observed that the amount of collagen in the EGF-treated group was larger than the control group. In the EGF-treated group, the visible external scars were less noticeable than that in the control group. These results suggest that EGF can reduce cutaneous scars by suppressing inflammatory reactions, decreasing expression of TGF-beta1, and mediating the formation of collagen.
Animals ; Cicatrix/pathology/*prevention & control ; Collagen/metabolism ; Epidermal Growth Factor/*pharmacology ; Humans ; Inflammation/metabolism ; Mice ; Recombinant Proteins/*pharmacology ; Skin/drug effects/metabolism/pathology ; Wound Healing/*drug effects

BACKGROUNDSmoking is the major cause of airway inflammation in chronic obstructive pulmonary disease (COPD), and smoking cessation is regarded as one of the important strategies for prevention and treatment of the inflammation. The inflammation of the chronic airway may be present and deteriorated even if the COPD patients stop smoking. Whether and how early smoking cessation affects the progress of inflammation is still obscure. This study was conducted to find the appropriate time for smoking cessation to terminate the airway inflammation in rats with smoke-induced chronic bronchitis.

METHODSA rat model of COPD was established by passively inhaling smoke mixture. Fifty-four young male Sprague-Dawley rats were randomly divided into 9 groups with different periods of smoke exposure and different time points of cessation. The inflammation markers to be detected included inflammatory cells in the bronchoalveolar lavage fluid (BALF), the myeloperoxidose (MPO) activity, the morphologic changes and the expression of ICAM-1 on the airway epithelium.

RESULTSWhen smoking was terminated at early stage, the inflammatory markers and related indexes were different from those of the typical chronic bronchitis group (group M7) (P < 0.01). The pathologic score of group SC7 (2 weeks of smoking cessation after occurrence of typical chronic bronchitis) was not different from that of group M7, and the level of ICAM-1 was still up-regulated (compared to group M7, P > 0.05). Meanwhile, most of inflammatory cells in BALF were neutrophils compared to other groups (P < 0.01). When smoking was terminated, the MPO activity was significantly lower than that of group M7 (P < 0.01).

CONCLUSIONSSmoking cessation at early stage can effectively inhibit the inflammatory reaction of COPD. Once chronic bronchitis occurs, little could be improved by smoking cessation.

Animals ; Bronchitis ; pathology ; Chronic Disease ; Inflammation ; prevention & control ; Intercellular Adhesion Molecule-1 ; analysis ; Lung ; pathology ; Male ; Neutrophils ; physiology ; Peroxidase ; metabolism ; Rats ; Rats, Sprague-Dawley ; Smoking Cessation

Inflammation of the asthmatic airway is usually accompanied by increased vascular permeability and plasma exudation. Angiopoietin-1 (Ang1) has potential therapeutic applications in preventing vascular leakage. Recently, we developed a soluble, stable, and potent Ang1 variant, COMP-Ang1. COMP-Ang1 is more potent than native Ang1 in phosphorylating the tyrosine kinase with immunoglobulin and epidermal growth factor homology domain 2 receptor in lung endothelial cells. We have used a mouse model for allergic airway disease to determine effects of COMP-Ang1 on allergen-induced bronchial inflammation and airway hyper-responsiveness. These mice develop the following typical pathophysiological features of allergic airway disease in the lungs: increased numbers of inflammatory cells of the airways, airway hyper-responsiveness, increased levels of Th2 cell cytokines (IL-4, IL-5, and IL-13), adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1), and chemokines (eotaxin and RANTES), and increased vascular permeability. Intravenous administration of COMP-Ang1 reduced bronchial inflammation and airway hyper-responsiveness. In addition, the increased plasma extravasation in allergic airway disease was significantly reduced by the administration of COMP-Ang1. These results suggest that COMP-Ang1 attenuates airway inflammation and hyper-responsiveness, prevents vascular leakage, and may be used as a therapeutic agent in allergic airway disease.
Allergens/immunology ; Angiopoietin-1/genetics/pharmacology/*therapeutic use ; Animals ; Asthma/*prevention & control ; Bronchial Hyperreactivity/physiopathology/prevention & control ; Chemokines/metabolism ; Inflammation/pathology/*prevention & control ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/*therapeutic use

Cytokines ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; HMGB1 Protein ; metabolism ; Humans ; Immunity, Cellular ; Inflammation Mediators ; metabolism ; Sepsis ; complications ; drug therapy ; pathology ; prevention & control ; Wounds and Injuries ; complications ; drug therapy ; pathology ; prevention & control

OBJECTIVETo investigate the effect of H₂S on lower limb ischemia-reperfusion (LIR) induced lung injury and explore the underlying mechanism.

METHODSWistar rats were randomly divided into control group, IR group, IR+ Sodium Hydrosulphide (NaHS) group and IR+ DL-propargylglycine (PPG) group. IR group as lung injury model induced by LIR were given 4 h reperfusion following 4 h ischemia of bilateral hindlimbs with rubber bands. NaHS (0.78 mg/kg) as exogenous H₂S donor and PPG (60 mg/kg) which can suppress endogenous H₂S production were administrated before LIR, respectively. The lungs were removed for histologic analysis, the determination of wet-to-dry weight ratios and the measurement of mRNA and protein levels of aquaporin-1 (AQP₁), aquaporin-5 (AQP₅) as indexes of water transport abnormality, and mRNA and protein levels of Toll-like receptor 4 (TLR₄), myeloid differentiation primary-response gene 88 (MyD88) and p-NF-κB as indexes of inflammation.

RESULTSLIR induced lung injury was accompanied with upregulation of TLR₄-Myd88-NF-κB pathway and downregulation of AQP1/AQP₅. NaHS pre-treatment reduced lung injury with increasing AQP₁/AQP₅ expression and inhibition of TLR₄-Myd88-NF-κB pathway, but PPG adjusted AQP₁/AQP₅ and TLR4 pathway to the opposite side and exacerbated lung injury.

CONCLUSIONEndogenous H₂S, TLR₄-Myd88-NF-κB pathway and AQP₁/AQP₅ were involved in LIR induced lung injury. Increased H₂S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR₄-Myd88-NF-κB pathway and AQP₁/AQP₅ expression to reduce inflammatory reaction and lessen pulmonary edema.

Acute Lung Injury ; complications ; pathology ; prevention & control ; Animals ; Aquaporins ; metabolism ; Drug Evaluation, Preclinical ; Edema ; etiology ; pathology ; Hydrogen Sulfide ; pharmacology ; therapeutic use ; Inflammation ; prevention & control ; Lung ; pathology ; Male ; Myeloid Differentiation Factor 88 ; metabolism ; NF-kappa B ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; complications ; pathology ; prevention & control ; Toll-Like Receptor 4 ; metabolism ; Water ; metabolism

Atherosclerotic cardiovascular disease (ASCVD) is the deadliest disease in the world, with endothelial injury occurring throughout the course of the disease. Therefore, improvement in endothelial function is of essential importance in the prevention of ASCVD. Red yeast rice (RYR), a healthy traditional Chinese food, has a lipid modulation function and also plays a vital role in the improvement of endothelial reactivity and cardiovascular protection; thus, it is significant in the prevention and treatment of ASCVD. This article reviews the molecular mechanisms of RYR and its related products in the improvement of endothelial function in terms of endothelial reactivity, anti-apoptosis of endothelial progenitor cells, oxidative stress alleviation and anti-inflammation.
Apoptosis ; drug effects ; Atherosclerosis ; pathology ; physiopathology ; prevention & control ; Biological Products ; chemistry ; pharmacology ; therapeutic use ; Cardiovascular Diseases ; pathology ; physiopathology ; prevention & control ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; therapeutic use ; Endothelium, Vascular ; cytology ; drug effects ; physiology ; Humans ; Inflammation ; prevention & control ; Lipid Metabolism ; drug effects ; Oxidative Stress ; drug effects

OBJECTIVETo investigate the effect of Modified Zhuye Shigao Decoction (MZSD) and its components on preventing radiation esophagitis of rats.

METHODSOne hundred Wistar rats were randomly divided into 5 groups, including the control group, radiation model group, MZSD group, Zhuye Shigao Decoction (ZSD) group, and added ingredients group, 20 rats in each group. The model of radiation esophagitis of rat was established by once local radiation of 40 Gy (330 Mu/min) with a high energy linear accelerator. The administration of Chinese medicine was continued for 14 days from 7 days before radiation application in the three treatment groups. On the 7th and 14th day, the serum was isolated and the levels of inflammatory cytokines tumor necrosis factor (TNF-α), interleukin 1β (IL-1β) and IL-8 were tested. The pathological slices of esophagus were obtained, and the pathological changes were observed. During the whole process, weight and food intake were recorded each day.

RESULTSOn the 7th day after radiation, the esophagus of rats in the MZSD group was almost intact, and the pathological injury score was significantly lower than that of the radiation model group, ZSD group and added ingredients group (P<0.01). Compared with the control group, the body weight and food intake of rats in the radiation model group were significantly decreased, and the levels of TNF-α, IL-1β and IL-8 were significantly increased (P<0.05 or P<0.01), while the MZSD group showed a significant increase in body weight and food intake, and a significant decrease in the levels of TNF-α, IL-1β and IL-8 compared with the radiation model group, ZSD group and added ingredients group (P <0.05 or P<0.01).

CONCLUSIONMZSD prevents the development of radiation esophagitis probably by inhibiting the generation and release of the inflammatory cytokines TNF-α, IL-1β and IL-8.

Animals ; Body Weight ; drug effects ; Cytokines ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Esophagitis ; drug therapy ; pathology ; prevention & control ; Esophagus ; drug effects ; pathology ; Feeding Behavior ; drug effects ; Inflammation Mediators ; metabolism ; Male ; Neutrophil Infiltration ; drug effects ; Radiation Injuries ; drug therapy ; pathology ; prevention & control ; Rats, Wistar ; Time Factors