• Applied Microscopy
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• v.32 no.4
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• pp.361-376
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• 2002

This research was conducted to determine the effects of chitosanoligosaccharide on liver poisoning induced by cadmium (Cd). Three groups of mice were used in this research. The group was only injected with cadmium (5.0 mg/kg; i.p.) (group Cd) and the other group was injected with cadmium and chitosanoligosaccharide (0.5% solution) at the same time (group Cd+Chi). In order to investigate the inhibitory action of chitosanoligosaccharide on liver damage, cadmium concentration in liver tissues and metallothionein (MT) concentration were relatively measured. In addition, histological observations were made to determine the morphologic injury of liver tissues. Cadmium concentration in liver tissues was drastically lower in groups Cd+Chi than in group Cd. MT concentration in liver tissues was lower in group Cd than in groups Cd+Chi. As the result of electron microscopic observation, mitochondria in group Cd showed a severe swelling phenomenon, RER fragment and ribosome dropout. However, in groups Cd+Chi, mitochondria with high electron density were distributed and RER forming a typical lamellae with ribosome was observed. From these results, cadmium toxicity on rat liver tissues could be lessened by chitosanoligosaccharide.

• Toxicological Research
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• v.34 no.1
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• pp.1-6
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• 2018

The purpose of this study was to detect cell death in the liver of mice treated with thioacetamide (TAA) using fluorescence bioimaging and compare this outcome with that using conventional histopathological examination. At 6 weeks of age, 24 mice were randomly divided into three groups: group 1 (G1), control group; group 2 (G2), fluorescence probe control group; group 3 (G3), TAA-treated group. G3 mice were treated with TAA. Twenty-two hours after TAA treatment, G2 and G3 mice were treated with Annexin-Vivo 750. Fluorescence in vivo bioimaging was performed by fluorescence molecular tomography at two hours after Annexin-Vivo 750 treatment, and fluorescence ex vivo bioimaging of the liver was performed. Liver damage was validated by histopathological examination. In vivo bioimaging showed that the fluorescence intensity was increased in the right upper part of G3 mice compared with that in G2 mice, whereas G1 mice showed no signal. Additionally ex vivo bioimaging showed that the fluorescence intensity was significantly increased in the livers of G3 mice compared with those in G1 or G2 mice (p < 0.05). Histopathological examination of the liver showed no cell death in G1 and G2 mice. However, in G3 mice, there was destruction of hepatocytes and increased cell death. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining confirmed many cell death features in the liver of G3 mice, whereas no pathological findings were observed in the liver of G1 and G2 mice. Taken together, fluorescence bioimaging in this study showed the detection of cell death and made it possible to quantify the level of cell death in male mice. The outcome was correlated with conventional biomedical examination. As it was difficult to differentiate histological location by fluorescent bioimaging, it is necessary to develop specific fluorescent dyes for monitoring hepatic disease progression and to exploit new bioimaging techniques without dye-labeling.

• The Journal of Internal Korean Medicine
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• v.27 no.1
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• pp.1-15
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• 2006

Objective : This study was done to investigate the effect of KJT on hypertension. Methods : Spontaneous Hypertensive Rats were sensitized and challenged with Kamijaeumganghwatang(KJT) for 5 weeks. Experimental group was treated with $200mg/day/2m{\ell}$ of KJT orally and control group was treated with $2m{\ell}/day$ of normal saline instead. Results : 1. KJT significantly showed significant protection against cytotoxicity and toxicity in the liver and the kidney. 2. KJT significantly decreased the blood pressure in SHR. 3. KJT significantly decreased the levels of aldosterone in SHR. 4. KJT significantly decreased the levels of dopamine, norepinephrine and epinephrine in SHR. 5. KJT significantly decreased the levels of sodium and potassium in SHR, but it did not decrease the levels of chloride in SHR. Levels of calcium in SHR increased, but only insignificantly. 6. KJT significantly decreased the levels of IL-6 in SHR, and significantly increased the levels of IL-10 in SHR. 7. For histological effects, KJT dillated capillary vessels in the kidney, significantly decreased eosinophilic changes in heart cells, and significantly decreased endothelial damage in the aorta. Conclusion: These results suggest that KJT is useful in treatment of hypertension.

• The Journal of Internal Korean Medicine
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• v.27 no.1
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• pp.72-83
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• 2006

Objective : This study was designed to identify lipid protection formation in stratum corneum and anti-inflammatory effects of Sopungdojeok-tang(SD) on atopic dermatitis(AD). Materials and Methods : In Vivo, SD extract was orally administered to BALB/c mice at $2.5m{\ell}/kg/day$ for 2 days after 5% sodium dodecyl sulfate evoked atopic dermatitis in abdominal skin. Morphological changes were observed by immunohistochemical stain using monoclonal antibodies(BrdU, ceramide, MIP-2, $NF-{\kappa}B$ p50, IL-4, and STAT6) and TUNEL method. In vitro, the alterations of IL-4 mRNA expression were detected by RT-PCT in SD extract treated EL4 cells after phorbol-12-myristate-13-acetate and 4-tert-Octylphenol induce Th2 skewed condition. Results : SD is used in Oriental Medicine for its potential curative for atopic dermatitis. In this study, we have investigated the anti-inflammatory and lipid lamella repair effects of SD were investigated. SD decreased the number of eosinophil in atopic dermatitis induced mice. In the histological properties, the hyperplasia, edema, infiltration of lymphocytes, damage of intercellular space of stratum corneum, BrdU positive reacted cells in stratum basal, and degranulated mast cells and capillaries in dermal papillae decreased in mice with SD. Treatment of SD also decreased MIP-2, STAT6 and IL-4 in dermal papillae. The IL-4 mRNA expression decreased in a dose-dependant manner in SD treated EL4 cells. In addition, decrease of $NF-{\kappa}B$ p50 and increase of apoptotic cells in dermis were observed in SD treated mice. These data suggest that SD may beneficial for atopic dermatitis. Conclusions : These data suggest that SD is beneficial in treatment of atopic dermatitis, and that SD provides lipid protection in stratum corneum and anti-inflammatory effects on atopic dermatitis.

• The Journal of Korean Physical Therapy
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• v.15 no.2
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• pp.182-195
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• 2003

This study investigated the effects of triamcinolone acetonide by iontophoretic transdermal drug delivery on anti-inflammatory action into the rats and which had carrageenan-induced hyperalgesia and edema in the feet, trauma-induced tissue damage in the thigh. Each group was treated under the fellowing conditions. 1. Group I : Control group 2. Group II : Application of direct current 3. Group III : Application of 0.1$\%$ triamcinolone acetonide solution 4. Group IV : Iontophoresis of 0.1$\%$ triamcinolone acetonide solution The degree of anti-inflammation was evaluated by the paw withdrawal latency, the change in volume of foot the change of paw edema, histological change in rats. 1. In paw withdrawal latency, group IV showed the most significant therapeutic effect than the other groups at 0, 3, 6 and 9 hours(p < 0.001). 2. In paw edema experiment in the foot, group IV showed the most significant effect than group I at 0, 3, 6 and 9 hours. It meant that there was effective anti-inflammatory reaction in group I (p < 0.001). 3. In the light microscopic observation, group IV showed the most significant reduction of haemorrhage, hyperemia and infiltrative inflammation. From the results, the iontophoresis with triamcinolone acetonide is more effective than using each groups. It is one of the effective physical agent which delivered large molecular weight drug into the body. The continuous study is needed for many interesting issues of iontophoretic transdermal drug delivery in new future.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.576-583
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• 2018

Human rhinoviruses (HRV) are one of the major causes of common cold in humans and are also associated with acute asthma and bronchial illness. Heat-shock protein 90 (Hsp90), a molecular chaperone, is an important host factor for the replication of single-strand RNA viruses. In the current study, we examined the effect of the Hsp90 inhibitor pochonin D, in vitro and in vivo, using a murine model of human rhinovirus type 1B (HRV1B) infection. Our data suggested that Hsp90 inhibition significantly reduced the inflammatory cytokine production and lung damage caused by HRV1B infection. The viral titer was significantly lowered in HRV1B-infected lungs and in Hela cells upon treatment with pochonin D. Infiltration of innate immune cells including granulocytes and monocytes was also reduced in the bronchoalveolar lavage (BAL) by pochonin D treatment after HRV1B infection. Histological analysis of the lung and respiratory tract showed that pochonin D protected the mice from HRV1B infection. Collectively, our results suggest that the Hsp90 inhibitor, pochonin D, could be an attractive antiviral therapeutic for treating HRV infection.

• Korean Journal of Environmental Agriculture
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• v.14 no.3
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• pp.282-288
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• 1995

To investigate the alterations in the ultrastructure of leaves by acid rain, 10mm of SAR(Simulated Acid Rain, pH 2.0, 2.7, 3.0, 6.0) was applied to three crops(red-pepper, perilla, eggplant) at a two-day interval. The symptoms of leaf damage by SAR were observed by naked eyes and SEM(Scanning Electron Microscope), and the peroxidase activity in the leaves was measured. The results are summarized as follows : The severity of SAR damages to the crops observed by naked eye were in the decreasing order of red-pepper, perilla, and eggplant. The Symptoms were characterized by brown or white spots on the leaf surface. In the SAR treatment of pH 3.0, trichomes of all crops except for eggplant were damaged. By the SAR treatment of pH 2.7, stomata were damaged in all crops. With one time treatment of SAR, the peroxidase activity of perilla was rapidly increased.

• Childhood Kidney Diseases
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• v.13 no.2
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• pp.99-117
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• 2009

Diabetic nephropathy is a major cause of chronic renal failure in developing countries, and the prevalence rate has markedly increased during the past decade. Diabetic nephropathy shows various specific histological changes not only in the glomeruli but also in the tubulointerstitial region. In the early stage, the effacement of podocyte foot processes and thickened glomerular basement membrane (GBM) is noticed even at the stage of microalbuminuria. Nodular, diffuse, and exudative lesions, so-called diabetic glomerulosclerosis, are well known as glomerular lesions. Interstitial lesions also exhibit fibrosis, edema, and thickened tubular basement membrane. Diabetic nephropathy is considered to be multifactorial in origin with increasing evidence that one of the major pathways involved in the development and progression of diabetic nephropathy as a result of hyperglycemia. Hyperglycemia induces renal damage directly or through hemodynamic alterations, such as, glomerular hyperfiltration, shear stress, and microalbuminuria. Chronic hyperglycemia also induces nonhemodynamic dysregulations, such as, increased production of advanced glycosylation endproducts, oxidative stress, activation of signal pathway, and subsequent various cytokines. Those pathogenic mechanisms resulted in extracellular matrix deposition including mesangial expansion and GBM thickening, glomerular hypertrophy, inflammation, and proteinuria. In this review, recent opinions on the histopathologic changes and pathophysiologic mechanisms leading to initiation and progression of diabetic nephropathy will be introduced.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.4
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• pp.409-415
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• 2013

We attempted to determine the action target of Shiitake mushroom extract with a known anti-hyperlipidemic effect in poloxamer(P) 407-induced hyperlipidemia model. We investigated the anti-hyperlipidemic effects of the water extract from Shiitake mushroom on the progress of high fat diet for 4 weeks. Experimental rats were divided into 5 different experimental groups including an normal group (normal diet; n=10), control group (hyperlipidemia; n=10), Experimental group I (hyperlipidemic rats treated with Shiitake mushroom extract (100 mg/kg, PO), n=10), Experimental group II (hyperlipidemic rats treated with Shiitake mushroom extract (300 mg/kg, PO), n=10), and Experimental group III (hyperlipidemic rats treated with Shiitake mushroom extract (500 mg/kg, PO), n=10). It is to analysis changes in body weight, visceral fat weight, blood lipid profiles, HMG-CoA reductase and histological findings. Body weight and epididymal fat weight was not significantly change in experimental groups (p>0.05). The level of total cholesterol, TG, arthrogenic index, and HMG-CoA reductase were significantly lower in experimental groups than control group (p<0.05). These results suggested that the Shiitake mushroom extract administration may act by inhibitory the release of cholesterol related factors and HMG-CoA from the hepatocyte without liver and kidney cell damage in hyperlipidemia rats.

• Toxicological Research
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• v.34 no.2
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• pp.143-150
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• 2018

It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.