• Archives of Plastic Surgery
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• v.37 no.2
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• pp.110-114
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• 2010

Purpose: On this study, we investigated the effects of curcumin and adipose-derived stromal cells (ADSCs) in wound healing process, especially in the aspect of synergic effects when they were administrated simultaneously. Methods: Curcumin (40 mg/kg) and/or $1.0{\times}10^6$ ADSCs were applied to an $1.5{\times}1.5\;cm$-sized full thickness wound on the backs of male Lewis rats (n=5 in each group). In control group (n=5), saline was administrated instead of curcumin and ASCs. The wound size was followed by computer planimetry in 5, 7, and 14 days, and wounds were harvested for histological analysis in 7 and 14 days. Results: The dimensions of wounds of curcumin, ADSCs, and curcumin-ADSCs group significantly decreased in 5, 7, 14 days compared with those of control group (p<0.05), but there were no significant differences among three groups. The wound sizes were lowest in curcumin-ADSCs group compared with the other groups, but the differences were insignificant (p>0.05). There were infiltration of more epithelization and more precisely organization of extracellular matrix in curcumin, ADSCs, and curcumin-ADSCs group compared with those of control group. Conclustion: The results suggest that curcumin and ADSCs have beneficial effects in the acceleration of wound healing. Although the simultaneous application of curcmin and ADSCs also has beneficial effects on wound healing, there are no significant synergic effects.

• Journal of Korean Medicine Rehabilitation
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• v.21 no.1
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• pp.79-95
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• 2011

Objectives : This study was to investigate the antiarthritic effect of Hwallak-dan(Huoluo-dan) on the complete freund's adjuvant(CFA)-induced arthritis in Lewis rats. Methods : Arthritis was induced by intradermal injection of CFA into base of tail. Experimental groups divided into normal(n=10), control(n=10) and treated(n=10) group. Animals of control group received normal saline for twenty days, treated group received extracts Hwallak-dan(Huoluo-dan) for same duration, light mineral oil only injected non-arthritic rats were served as normal group. The incidence of arthritis and arthritic index were observed after treatment. Body weight, paw edema volume and thickness of ankle joint were measured at 0, 11, 14, 17, 20 days after treatment. White blood cell(WBC) counts in blood were analysed at 20 days after treatment and tumor necrosis $factor-{\alpha}(TNF-{\alpha})$, $interleukin-1{\beta}(IL-1{\beta}$), IL-6 contents in paw exudate were analysed by ELISA at 20 days after treatment. Histopathology on the ankle joint were performed at 20 days after treatment. Results : 1. Incidence of arthritis of treated group was 60% and control group was 100% at 20 days after treatment. 2. Arthritic index of treated group was significantly decreased compared with control group at 20 days after treatment. 3. Paw edema volume and thickness of ankle joint of treated group was significantly decreased compared with control group at 20 days after treatment. 4. Total WBC of treated group was significantly decreased compared with control group at 20 days after treatment. 5. Neutrophils of treated group was significantly decreased compared with control group at 20 days after treatment. 6. $TNF-{\alpha}$ content in paw exudate of treated group was significantly decreased compared with control group at 20 days after treatment. 7. $IL-1{\beta}$ content content in paw exudate of treated group was significantly decreased compared with control group at 20 days after treatment. 8. IL-6 content content in paw exudate of treated group was significantly decreased compared with control group at 20 days after treatment. 9. Histopathological arthritic index of treated group was significantly decreased compared with control group at 20 days after treatment. Conclusions : These results indicate that Hwallak-dan(Huoluo-dan) has inhibitory effect on the development and progression of CFA-induced arthritis in rats.

• The Journal of Korean Medicine
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• v.23 no.4
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• pp.98-104
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• 2002

Objectives: Calpain, a calcium-dependent cysteine proteinase, may be one of the proteolytic enzymes that mediate cartilage degradation associated with rheumatoid arthritis. The object of this study is to ascertain immunohistochemically whether calpain is present in the inflamed joints of collagen-induced arthritis of rats, and examine the effect of Cortex Acanthopanacis Senticosi on the expression of calpain. Methods: Male Lewis rats, around 200g of body weight, were immunized with bovine type II collagen. After 3 weeks from first immunization, rats were divided into arthritic control (n=6) group and Cortex Acanthopanacis Senticosi-treated (n=6) group. Non-immunized rats served as the normal (n=6) group. All animals were sacrificed at 15 days post-treatment and tibiotarsal joints were removed. Calpain immunohistochemistry was performed on the midsagittal section of the tibiotarsal joint. Results: All animals of the control and treated groups showed ankylosing osteoarthritis. However, the animals of the treated group showed alleviation in the fibrous ankylosis, destruction of articular cartilage and destruction of subchondral bony tissue compared with the animals of the control group. Calpain was expressed in the chondrocyte lacunae of growing articular cartilage, in the skeletal muscle fibers, in the peripheral nerves, and in the vessel walls around the joints of all groups. In the control and treated groups, calpain was also expressed in proliferating synovial epithelia, subsynovial stroma cells, surface of articular cartilage, and fibrous pannus around destructive subchondral bony tissue. However, the expression density of calpain in the treated group was diminished compared with the control group, especially in surface of articular cartilage and fibrous pannus. Conclusions: These observations indicated that calpain plays an important role in the destruction of cartilage and bone in collagen-induced arthritis of rats, and also indicated that Cortex Acanthopanacis Senticosi inhibits the development of arthritis by decreasing the expression of calpain.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.2
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• pp.103-111
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• 2019

The study is to investigate effects of andrographolide on experimental autoimmune myocarditis (EAM). Lewis rats were immunized on day 0 with porcine cardiac myosin to establish EAM. The EAM rats were treated with either andrographolide (25, 50, 100 mg/kg/day) or vehicle for 21 days. An antigen-specific splenocytes proliferation assay was performed by using the cells from control rats immunized with cardiac myosin. Survival rates, myocardial pathology and myocardial functional parameters (left ventricle end-diastolic pressure, ${\pm}dP/dt$ and left ventricular internal dimension) of EAM rats received andrographolide were significantly improved. Andrographolide treatment caused an decrease in the infiltration of $CD3^+$ and $CD14^+$ positive cells in myocardial tissue. Moreover, andrographolide treatment caused a reduction in the plasma levels of tumor necrosis factor-alpha, interleukin-17 (IL-17) and myosin-antibody, and an increase in the level of IL-10 in EAM rats. Oral administration of andrographolide resulted in the decreased expression of p-PI3K, p-Akt without any change of PI3K and Akt. Further results indicate andrographolide significantly inhibited myosin-induced proliferation in splenocytes, and this effect was inhibited by co-treatment of SC79 (Akt activator). Our data indicate andrographolide inhibits development of EAM, and this beneficial effect may be due to powerful anti-inflammatory activity and inhibitory effect on PI3K/Akt pathway.

• Korean Journal of Veterinary Research
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• v.45 no.1
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• pp.7-15
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• 2005

To elucidate the roles of phospho-IkB expression in the development and progression of EAE, we investigated the expression of phospho-IkB in the central nervous system (CNS) of rats during experimental autoimmune encephalomyelitis (EAE) using immunohistochemistry and Western blot analysis. In Western blot analysis, the increased expression of phospho-IkB went parallel to severity of EAE. The expression of phospho-IkB increased significantly at the peak stage of EAE followed by gradual decrease. Immunohistochemical studies showed that the phospho-IkB immunoreactivity was mainly expressed in inflammatory cells (macrophages, T cells) and glial cells (astrocytes, microglial cells) at the peak stage of EAE and disappeared at the recovery stage. These findings suggest that the phosphorylation of IkB is closely associated with autoimmune inflammation in the CNS and plays an important role in the initiation and progression of EAE.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.193-193
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• 1996

Endothelin-1, which is a peptide originally isolated from cultured porcine aortic cell, has been found to play a crucial role in potentiating the vasoconstriction mitogenesis, and chemotaxis. In the present study, we examined the level of endothelin-1 in the brain, spinal cord and blood from rat with experimental allergic encephalomyelitis(EAE). At the peak stage of EAE(grade 3), endothelin-1 level in the spinal cord of rat with EAE increased two folds as compared with that of sham-treated rats, and subsequently decreased to the level of control at the recovery stage. In the endothelin-1 immunocytochemistry, endothelin-1 immunopositive cells and ED-1, macrophage marker immunopositive cells observed in the spinal cord of peak stage(grade 3). These Findings suggest that endothelin-1 play the important role in progression of EAE.

• Korean Journal of Veterinary Research
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• v.40 no.3
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• pp.431-437
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• 2000

The aim of this study was to evaluate the involvement of CPP32 (caspase-3), one of the death-related enzymes, in the course of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats immunized with an emulsion of rat spinal cord homogenate with complete Freunds adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml). The expression of CPP32 in the spinal cords of rats with EAE was studied. In normal rat spinal cords, CPP32 is constitutively, but weakly, expressed in neurons and some neuroglial cells. In the EAE spinal cords, many inflammatory cells were positive for CPP 32, and the majority of CPP32(+) cells were identified as ED1(+) macrophages. During this stage of EAE, the number of CPP32(+) cells in brain cells, including neurons and astrocytes, increased, and these cells also had increased CPP32 immunoreactivity. CPP32 immunor eactivity was not always matched with apoptosis of inflammatory cells in EAE lesions. We speculate that CPP32, which is constitutlvely expressed in brain cells, increases in response to neuroimmunological stimulation in both brain neuronal cells and inflammatory cells. The functional role of CPP32 in neuroimmunological disorders is discussed.

• Korean Journal of Veterinary Pathology
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• v.1 no.1
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• pp.26-32
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• 1997

Protein kinase C an enzyme of signal transduction has been known to regulate cell proliferation activation as well as apoptosis in some cancer cell lines. To explore the role of PKC in the course of cell mediated autoimmune disease such as experimental autoimmune encephalomyelitis (EAE) EAE was induced in Lewis rats(6-8 weeks old) with immunization of myelin basic protein supplemented with complete Freund's adjuvants and affected spinal cords were sampled at days 13 postimmunization(PI) as peak stage of EAE and at days 21 PI as recovery stage. The spinal cords with EAE were subjected to Northern blot analysis and insitu hybridization of PKC delta which is one of prominant isotypes of PKC in the haematopoietic cells. Northern blot analysis showed that levels of PKS delta mRNA in the spinal cords of rats withEAE was significantly increased at days 13 PI in which inflammatory cells including T cells and macrophages in the EAE lesions appeared. however the stage. By in situ hybridization signals of PKC delta in EAE lesions was intensely expressed on the delta is also expressed on some brain cells in normal rat central nervous system This finding suggests that PKC plays an important role on either activation of inflammatory cells including encephalitogenic T cells and macrophages or apoptotic elimination of some inflammatory cells depending on the stge of EAE.

• Annals of Clinical Neurophysiology
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• v.1 no.2
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• pp.91-98
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• 1999

Background : The pathogenesis of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), Guillain Barre syndrome (GBS) is not clear, but it has been known that the immune mechanisms play an important role. Authors performed this study to establish an animal model of experimental allergic neuritis (EAN) by immunizing the myelin components of peripheral nerves and to understand the electrophysiological and histopathological features as well as the ${CD_5}^+$ B-lymphocyte changes in peripheral bloods in the EAN models. Methods : Lewis rats weighing 150-200 gm were injected subcutaneously in soles two times with total myelin, P0, P1, or P2 proteins purified from the bovine cauda eguina. The EAN induction was assessed by evaluating clinical manifestations. The electrophysiological and histopathological features were studied as routine methods. The ${CD_5}^+$ Blymphocytes were double stained using monoclonal FITC conjugated anti-rat CD45RA and R-PE conjugated anti-rat ${CD_5}^+$ antibodies and calculated using a fluorescence activated cell sorter (FACS). Results : The EAN animal models were established. In two out of five, in one out of two, in none out of three, and in none out of one Lewis rats injected with purified total myelin, P0, P1, P2 proteins respectively, They showed slow spontaneous motor activity and weak resistance against pulling back by tails. The typical electrophysiological and histologic findings in total protein and P0 induced EAN animal models were the decreased conduction velocity, the decreased compound muscle action potential (CMAP) amplitude and the dispersion phenomenon. The perivascular infiltrates of lymphocytes with focal demyelinating process were found in light microscopy. The ${CD_5}^+$ B-lymphocyte expression in three EANs were 2.38%, 3.50% 2.50%, which were not significantly increased, compared with those in normal controls. Conclusion : The EAN animal models were successfully established by injecting the total myelin and P0 myelin and they showed electrophysiological and histological features typical of demyelinating process. However they did not show an increased expression of ${CD_5}^+$ B-lymphocyte in peripheral bloods which could be indirect evidence of humoral autoimmunity.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.305-311
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• 2007

Glucocorticoids (GCs) alter metabolism, synaptogenesis, apoptosis, neurogenesis, and dendritic morphology in the hippocampus. To better understand how glucocorticoids regulate these aspects of hippocampal biology, we studied gene expression patterns in the CA3 (Hippocampal pyramidal cell field CA3) and dentate gyrus (DG). Litter-matched Lewis inbred rats treated for 20 days with either 9.5 mg per day sustained-release corticosterone or placebo pellets were compared with high-density oligonucleotide microarray analysis (Rat Neurobiology U34 Arrays, Affymetrix). In placebo-treated rats, 32 genes were expressed at greater levels in CA3 than DG, whereas 3 genes were expressed at great levels in DC than CA3. Regional differences were also apparent in corticosterone-induced changes in the hippocampal transcriptome. Six genes in CA3 and 41 genes in DC were differentially regulated by corticosterone. As per the glucocorticoid effects on gene transcription in the brain, forty three of these genes were upregulated, and 4 genes were downregulated. Genes differentially expressed in hippocampus included those for 13 neurotransmitter proteins, 5 ion channel related proteins, 4 transcription factors, 3 neurotrophic factors, 1 cytokine, 1 apoptosis related protein, and 5 genes involved in synaptogenesis. Interestingly, GCs can have suppressive effects on brain BDNF mRNA transcription, one of the neurotrophic factors. These results indicate the diversity of targets affected by chronic exposure to corticosterone and highlight important regional differences in hippocampal neurobiology.