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Silica Induced Early Fibrogenic Reaction in Lung of Mice Ameliorated by nyctanthes arbortristis Extract

Biomedical and Environmental Sciences 2002年第3期15卷 215-222页

作者： BHOLA NATH PAUL ANAND PRAKASH SIRISH KUMAR AJAY KYADAV UMANI ASHOK KSAXENA ANAND PRAKASH SAHU KEWAL LAL KALYAN KDUTTA Immunobiology Laboratory Industrial Toxicology Research CentreM.G.MargLucknow 226001U.P.India Inhalation Toxicology Laboratory Industrial Toxicology Research CentreM.G.MargLucknow 226001U.P.India Preventive Toxicology Laboratory Industrial Toxicology Research CentreM.G.MargLucknow 226001U.P.India

Objective To investigate the pharmacological effect of nyctanthes arbortristis (NAT) leaf extract in the prevention of lung injury induced by silica particles. Method Lung injury was induced in Swiss mice through inhalation exposure to silica particles (<5m) using a Flow Past Nose Only Inhalation Chamber at the rate of -10 mg/m3 respirable mass for 5 h. Lung bronchoalveolar lavage (BAL) fluid collected between 48 and 72 h was subjected to protein profiling by electrophoresis and cytokine evaluation by solid phase sandwich ELISA. Lung histopathology was performed to evaluate lung injury. Results Inhalation of silica increased the level of tumor necrosis factor-a (TNF-a), and of the 66 and 63 kDa peptides in the BAL fluid in comparison to sham-treated control. Pre-treatment of silica exposed mice with NAT leaf extract significantly prevented the accumulation of TNF-a in the BAL fluid, but the 66 and 63 kDa peptides remained unchanged. The extract was also effective in the prevention of silica-induced early fibrogenic reactions like congestion, edema and infiltration of nucleated cells in the interstitial alveolar spaces, and thickening of alveolar septa in mouse lung. Conclusion NAT leaf extract helps in bypassing silica induced initial lung injury in mice.

关键词： nyctanthes arbortristis Lung-injury Silica Mice prevention

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Comparative Studies of Different Organs of nyctanthes arbortristis in Modulation of Cytokines in Murine Model of Arthritis

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Biomedical and Environmental Sciences 2007年第2期20卷 154-159页

作者： BRIJESH RATHORE BHOLANATH PAUL BHUSAN P CHAUDHURY ASHOK KUMAR SAXENA ANAND PRAKASH SAHU YOGENDRA KUMAR GUPTA Immunobiology Laboratory Central Pathology Laboratory Preventive Toxicology Laboratory Industrial Toxicology Research Centre M. G. MargLucknow 226001India

Objective To study the modulation effect of pro- and anti-inflammatory cytokines following long term use of water soluble ethanol extracts from different organs of nyctanthes arbortristis （NAT） in mouse model of arthritis. Methods Arthritis was induced in mice by two injections of Freund＇s complete adjuvant on days 0 and 12 in the sub-planter surface of the right hind paw. Results Injection of adjuvant resulted in a maximum primary edema of the footpad with erythema, and edema and distortion of joints of the right hind paw after 24-48 hours. Second injection of FCA led to the formation of secondary swellings persisting more than four weeks that spread onto the other hind limb but to a lesser extent. Histological analysis of the ankle on day 47 showed marked evidence of cartilage destruction in association with pannus formation and moderate bone resorption. Proinfiammatory cytokine levels in the inflamed joint homogenate were elevated on days 2, 14, and 47. Oral administration of leaf and fruit extracts in arthritic mice reduced joint homogenate levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 on days 2, 14, and 47 in comparison to untreated arthritic mice. Intedeukin-10 level was elevated in the inflamed joint on days 2, 14, and 47 in comparisons to untreated arthritic mice. Confusion Evidence of lesser inflammation of the footpad and joint and associated histological observation support the therapeutic benefit of leaf and fruit extracts from nyctanthes arbortristis. This study helps in understanding the mechanism of anti-inflammatory action of nyctanthes arbortristis in the light of pro- and anti-inflammatory cytokine balance.

关键词： nyctanthes arbortristis Arthritis TNF-α IL- 1β IL-6 IL-10

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