• Applied Microscopy
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• v.34 no.1
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• pp.31-42
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• 2004

Acute respiratory distress syndrome (ARDS) is a kind of acute lung injury characterized by inflammatory disruption of alveolar-capillary barrier and notorious for its high mortality. Neutrophils cause cell damage through the production of free radicals, inflammatory mediators, and proteases in ARDS. $PLA_2$ might serve a primary regulatory role in the activation of neutrophils. This present study was performed to elucidate the effect of rutin known as $PLA_2$ inhibitor on ARDS induced by endotoxin. Endotoxin had increased lung myeloperoxidase (MPO) activity, BAL (bronchoalveolar lavage) protein content, numbers of neutrophils in BALF (bronchoalveolar lavage fluid) compared with those of control rat (p<0.001). In addition, histological evidence of lung injury was correlated with neutrophil influx into alveolar space and cerrous perhydroxide granules were found in lining of endothelial cell, alveolar type I, II cells. In contrast, pretreated group of rutin had significantly decreased all of the parameters (p<0.001). These data suggest that inhibition of $PLA_2$ is one step approach that block the process of ARDS. Accordingly, we conclude that rutin can be used as the prophylactic agent for ARDS on the bases of these experimental results.

• Journal of Ginseng Research
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• v.26 no.4
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• pp.191-195
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• 2002

In this study, we like to examine whether Panax ginseng water extract (PGWE) exerts antidiabetic activities in prevention and treatment modes in multiple low dose (MLD) streptozotocin (STZ) (20 mg/kg i.p injection for 5 days) induced diabetic SD rats. In the prevention mode,150 mg/kg of GRWE was administered intraperitoneally with STG for 3 weeks, and this group is called CO 150. In the treatment mode, we started to administer the same dose of PGWE on day 8 and for 3 weeks, and this group is called POST150. PGWE exerted significant hypoglycemic activities in both prevention (normal control, 97 ${\pm}$ 6 mg/dl; diabetic control, 331${\pm}$23; CO150, 211${\pm}$37) and treatment groups (normal control, 128${\pm}$4 mg/dl; diabetic control, 392${\pm}$33: POST150, 263${\pm}$44). Of great importance is the fact that plasma insulin levels in both groups were markedly increased as compared to the diabetic control (normal control,428.7${\pm}$62.1 pg/dl; diabetic control, 167.0${\pm}$91.7; CO150, 377.6${\pm}$68.7 in prevention mode, and in treatment mode normal control 417.9${\pm}$84.6 pg/dl; diabetic control, 166.1${\pm}$104.7; POST150, 315.2${\pm}$47.4). Blood glucose levels were closely associated with plasma insulin levels, and this result may suggest that PGWE showed the activity to enhance insulin secretion as well as preventing destruction of pancreatic islet cells. Food and water intakes were also determined at the last week of treatment i n both groups. Characteristic symptoms of diabetes were significantly improved in both groups. In the prevention mode, water intake (ml/rat/day) in normal control was increased from 30.6${\pm}$1.5 to 122.2${\pm}$3.4 in diabetic control rats. In the CO150-treated group, water intake was dramatically reduced to 68.3${\pm}$4.4 (p<0.001 vs. diabetic control). In the treatment mode, POST-treated group also reduced the water intake from 128.9${\pm}$2.2 to 113.3${\pm}$1.7. Taken together, our data suggest that PGWE showed comparable antidiabetic activities in prevention and treatment modes. Therefore, PGWE may have a potential as a prophylactic as well as therapeutic agent fur type 2 diabetes mellitus (T2DM).