Effect of spearmint oil on lipopolysaccharide induced emphysema-like changes and expression of matrix metalloproteinase-9 / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the effect of spearmint oil on emphysema-like changes and the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta(IL-1beta), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-9) in lipopolysaccharide (LPS) treated rats.</p><p><b>METHOD</b>Emphysematous changes model was induced by intratracheal instillation of LPS once a week for up to 8 weeks in rats. Rats were divided into control, dexamethasone (0.3 mg x kg(-1)), and spearmint oil (10, 30,100 mg x kg(-1)) groups. Each group was treated with saline, dexamethasone, and spearmint of oil respectively for 4 weeks. Then total and different white blood cell counts in bronchoalveolar lavage fluid(BALF) were carried out. The pathologic changes of lung tissue such as alveolar structure, airway inflammation, and goblet cell metaplasia were observed by HE and AB-PAS staining. Expression of TNF-alpha, IL-1beta, TIMP-1 and MMP-9 were measured.</p><p><b>RESULT</b>Both spearmint and dexamethasone decreased the destruction of pulmonary alveolus. The total and different white blood cell counts in BALF including neutrophile and lymphocyte of spearmint oil 100 mg x kg(-1) and dexamethasone group were significantly reduced, and the goblet cell metaplasia was also inhibited. Dexamethasone had inhibitory effect on the expression of TNF-alpha, IL-1beta, TIMP-1 and MMP-9. Spearmint oil 30, 100 mg x kg(-1) significantly reduced TNF-alpha and IL-1beta respectively. Spearmint oil 10, 30 and 100 mg x kg(-1) had no effect on the expression of TIMP-1, but could decrease the expression of MMP-9 significantly in lung tissues.</p><p><b>CONCLUSION</b>Spearmint oil has protective effect on rats with emphysematous changes, since it improves alveolar destruction, pulmonary inflammation, and goblet cell metaplasia. The mechanism may include reducing TNF-alpha, IL-1beta content and inhibiting overexpression of matrix metalloproteinase-9 in lung tissues.</p>

Inhibitory effects of 1,8-cineol on ovalbumin-induced lung inflammation and airway hyperresponsiveness in asthmatic guinea pigs / 中国药理学与毒理学杂志

OBJECTIVE To investigate the effects of 1,8-cineol on lung functions and mechanism in asthmatic guinea pigs. METHODS The guinea pig model was performed by intraperitoneal injection of the 0.5 ml Al(OH)_3 gel containing OVA 20 μg. The guinea pigs were constructed by immunization of intraperitoneal injection on the 0 day and the 7th day, and the experiment was performed on the 28th day. The effect of 1,8-cineol 10, 30 and 100 ml·kg~(-1) on the airway resistance(R_(aw)) and dynamic lung compliance (C_(dyn)) of asthmatic guinea pigs 1 h after challenge of OVA. The changes in leukocyte and different kinds of leukocyte in bronchoalveolar lavage fluid (BALF) after the challenge of OVA have been studied. The levels of eosinophil cationic protein (ECP), interleukin(IL)-4, IL-8 and tumor necrosis factor (TNF)-α in lungs of guinea pigs were determined using enzyme-linked immunosorbent assay (ELISA). The changes in R_(aw) and C_(dyn) of asthmatic guinea pigs were investigated 17 h after challenge of OVA and inhalated methacholine (MCh). The changes in leukocyte and different kinds of leukocyte in BALF after the challenge of OVA have been studied. The levels of ECP, IL-4, IL-8 and TNF-α in lungs of guinea pigs were determined using ELISA. RESULTS 1,8-Cineol inhibited increase in R_(aw) and decrease in C_(dyn) from 1 to 30 min after challenge of OVA in model group. The levels of ECP, IL-4 and TNF-α in asthmatic model group were higher than those in normal control group(P<0.05). The levels of ECP, IL-4 and TNF-α of 1,8-cineol 100 mg·kg~(-1) group were significantly lower than those in asthmatic model group (P<0.01). The level of IL-8 of asthmatic model group didn't have any significant difference from that of control group. 1,8-Cineol 100 mg·kg~(-1) could significantly decrease the numbers of leukocyte and the percent of eosinophils in BALF. Seventeen hours after challenge of OVA, R_(aw) and C_(dyn) of asthmatic model group were higher than these of control group (P<0.05, P<0.01); 1,8-cineol 100 mg·kg~(-1) significantly inhibited the increase in R_(aw), compared with model group (P<0.05); 1,8-cineol 10, 30 and 100 mg·kg~(-1) improved the decrease in C_(dyn) after MCh-induced in model group which were challenged by OVA after 17 h; 1,8-cineol 100 mg·kg~(-1) could significantly decrease the numbers of leukocyte and the percent of neutrophils, the levels of ECP, IL-8 and TNF-α compared with asthmatic group. The level of IL-4 in asthmatic model group didn't have any significant difference from that in normal control group. CONCLUSION In the course of early stage of asthma, 1,8-cineol inhibites the asthma by decreasing the number of eosinophils and down-regulating the activity of EPO. In the course of later stage of asthma, 1,8-cineol inhibits or improves the aggravation and lasting states of asthma which is directly coursed by neutrophils accumulating in the BALF that related to the increase in IL-8.

PHARMACOLOG1C STUDIES ON ?-CARYOPHYLLENE ALCOHOL / 中国药理学通报

?-caryophyllene was one of the effective antiasthmatic principles of essential oil of Artemisia argyi, by way of structural modification to form ?-caryophyllene alcohol. P-caryophyllene alcohol could protect acetylcholine and histamine-induced asthma in guinea pig, and the effect was longer than 4h. It had relaxant effect on isolated guinea pig tra.cheal smooth muscle prepareations, and the pD2 values was 4.36 + 0.37. The drug not only significantly inhibited antigen induced release of SRS-A in the lung fragments of sensitized guinea pig( ID50 23mg/L ), but also inhibited SRS-A induced contraction of the guinea pig ileum(ID50 18mg/L). In addition, P-caryophyllene alcohol had antitussive and expectora'at actions. These results show that p-caryophyllene alcohol is a new antiathmatic drug.