• Journal of Microbiology and Biotechnology
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• v.34 no.3
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• pp.606-621
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• 2024

This study evaluated the hepatoprotective effect of fermented Protaetia brevitarsis larvae (FPB) in ethanol-induced liver injury mice. As a result of amino acids in FPB, 18 types of amino acids including essential amino acids were identified. In the results of in vitro tests, FPB increased alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activities. In addition, FPB treatment increased cell viability on ethanol- and H₂O₂-induced HepG2 cells. FPB ameliorated serum biomarkers related to hepatoxicity including glutamic oxaloacetic transaminase, glutamine pyruvic transaminase, total bilirubin, and lactate dehydrogenase and lipid metabolism including triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Also, FPB controlled ethanol metabolism enzymes by regulating the protein expression levels of ADH, ALDH, and cytochrome P450 2E1 in liver tissue. FPB protected hepatic oxidative stress by improving malondialdehyde content, reduced glutathione, and superoxide dismutase levels. In addition, FPB reversed mitochondrial dysfunction by regulating reactive oxygen species production, mitochondrial membrane potential, and ATP levels. FPB protected ethanol-induced apoptosis, fatty liver, and hepatic inflammation through p-AMP-activated protein kinase and TLR-4/NF-κB signaling pathways. Furthermore, FPB prevented hepatic fibrosis by decreasing TGF-β1/Smad pathway. In summary, these results suggest that FPB might be a potential prophylactic agent for the treatment of alcoholic liver disease via preventing liver injury such as fatty liver, hepatic inflammation due to chronic ethanol-induced oxidative stress.

• 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).