The purpose of this study was to investigate the histochemical effect of Jojoongikgi-tang (JIT) on hairless mice induced by DNCB. For the study, DNCB was applied on the infrascapular region of the mices skin and then JIT was orally administered. As a result, the following histochemical changes of the dermis were observed through light and electron microscopes, and statistical data. The results obtained were as follows: 1. In the 2 days experimental group, more histamine mast cells dermis occurred than in the control or normal group when observed under light microscope. When an electron microscope was used, histochemical reactive cells in the dermis were found as mast cells that contained more cytoplasmic granules than in the control or normal group. 2. In the 5 days experimental group, the number of mast cells were decreased over the control or normal group when observed under light microscope. When an electron microscope was used, mast cells in the control contained secretory granules with higher electron density than those of the experimental group. 3. As a result of statistical analysis, the mean value of mast cells in the normal 2 days control and experimental groups was not significantly different (p<0.05). 4. However, the mean values of it in the normal ($19.1000{\pm}6.3154$), 5 day control ($103.4500{\pm}42.2704$) and 5 day experimental groups ($35.9500{\pm}8.5746$) were significantly different (p<0.05). From the above results, it is concluded that JIT is efficient against the purpura induced by DNCB.
Ku, Seo-kwang;Lee, Hyeung-sik;Kim, Jong-dae;Lee, Jae-hyun
Korean Journal of Veterinary Research
/
v.40
no.1
/
pp.153-165
/
2000
To identify, the effects of acua-acupuncture of Bletillae rhizoma extract on the duodenal ulcer induced by HCl-aspirin in rats, the changes of histological profiles, number of mucous-producing goblet cells (PAS-positive cells), and morphology and/or number of chole-cystokinin (CCK)-8 and serotonin-immunoreactive (IR) cells in the gastrointestinal tract were observed after acua-acupuncture of Bletillae rhizoma extract on Ganshu locus ($BL_{14}$). Samples were collected at 1, 3 and 5 days after treatment. Histologically, very severe injury, atrophy of villus, necrosis of epithelial cell and hemorrhage, to the duodenal mucosa including epithelium were observed in HCl-aspirin administrated control groups, and these injuries were increased with time intervals. But in acua-acupuncture groups and nontreated normal groups, no gross lesion of ulcer was demonstrated and histologically minor injury to the apex of villas epithelium was observed. Compared to the PAS-positive cells of the control groups, those of the acua-acupuncture groups were increased. Severe degranulation of CCK-8- and serotonin-IR cells were observed in the control groups but these phenomena seldom occur in the acua-acupuncture groups. Serotonin-IR cells were significantly decreased in control groups but increased in the acua-acupuncture groups compared to control groups. However, these degranulation of IR cells of the aqua-acupuncture groups were less severe than those of normal groups, and number of serotonin-IR cells were lower than those of normal groups but these phenomena were decreased with time intervals and in 5 days after treatment, they were observed like those of normal groups. These result indicated that acua-acupuncture of Bletillae rhizoma extract would be accelerated the healing of the duodenal ulcer but the functional mechanisms were unknown.
The brain maintains homeostasis and normal microenvironment through dynamic interactions of neurons and neuroglial cells to perform the proper information processing and normal cognitive functions. Recent post-mortem investigations and animal model studies demonstrated that the various brain areas such as cerebral cortex, hippocampus and amygdala have abnormalities in neuroglial numbers and functions in subjects with mental illnesses including schizophrenia, dementia and mood disorders like major depression and bipolar disorder. These findings highlight the putative role and involvement of neuroglial cells in mental disorders. Herein I discuss the physiological roles of neuroglial cells such as astrocytes, oligodendrocytes, and microglia in maintaining normal brain functions and their abnormalities in relation to mental disorders. Finally, all these findings could serve as a useful starting point for potential therapeutic concept and drug development to cure unnatural behaviors and abnormal cognitive functions observed in mental disorders.
In this study, nuclease-resistant RNA aptamers that are specific for Jurkat T leukemia cells were selected by a subtractive systemic evolution of ligands by exponential enrichment (SELEX) method. A randomized nuclease-resistant RNA library was incubated with normal peripheral blood mononuclear cells (PBMC) in each round to preclude RNAs that recognize the common cellular components on the surface of normal and cancer cells. The precluded RNAs were used for the selection of Jurkat T cell-specific aptamers, and the specific RNAs were then gradually enriched from start to the following selections. After 16 rounds of the subtractive SELEX, the selected aptamers were found to preferentially bind to Jurkat T cells, but not to the normal PBMC, evidenced by fluorescence-activated cell sorting analysis. Thus, the subtractive SELEX can be used to identify ligands to cancer-specific biological markers without prior knowledge of the nature of markers. The aptamers could be applied to specific cell sorting, tumor therapy, and diagnosis, and moreover, to find cancer cell-specific markers.
This study was designed to assess, whether a new chemotherapeutic microtubule inhibitor, Epothilone B (EpoB, Patupilone), can induce DNA damage in normal ovarian cells (MM14.Ov), and to evaluate if such damage could be repaired. The changes were compared with the effect of paclitaxel (PTX) commonly employed in the clinic. The alkaline comet assay technique and TUNEL assay were used. The kinetics of DNA damage formation and the level of apoptotic cells were determined after treatment with IC50 concentrations of EpoB and PTX. It was observed that PTX generated significantly higher apoptotic and genotoxic changes than EpoB. The peak was observed after 48 h of treatment when the DNA damage had a maximal level. The DNA damage induced by both tested drugs was almost completely repaired. As EpoB in normal cells causes less damage to DNA it might be a promising anticancer drug with potential for the treatment of ovarian tumors.
Journal of Physiology & Pathology in Korean Medicine
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v.16
no.4
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pp.714-719
/
2002
To examine effects of Whadamcheongwha-tang(WDCWT) extract, the mice investigated the gastrin and histamine secreting cells of the stomach by immunohistochemical method, and the lymphocytes of the spleen and thymus by flow cytometry after the oral administration of WDCWT extract(0.2ml/day) and omeprazole (1mg/day) for 7, 14 and 21 days. The result are as follows; 1. When WDCWT extract was administrated for 7 days, in result, gastrin secreting cells were unchanged. When omeprazole was administrated for 7 and 14 days, gastrin secreting cells were slightly increased than that of normal control group. When WDCWT extract was administrated for 21 days, in result, gastrin secreting cells were significantly increased 1.9 times than that of normal control group. When omeprazole was administrated for 21 days, gastrin secreting cells were increased 1.96 times than that of normal control group. 2. When WDCWT extract and omeprazole were administrated for 7 days, in result, histamine secreting cells were unchanged. When WDCWT extract was administrated for 21 days, in result, histamine secreting cells were significantly increased 1.9 times more than that of normal control group. When omeprazole was administrated for 21 days, in result, histamine secreting cells were increased 2.1 times compared with normal control group. 3. When WDCWT extract administrated for 7, 14 and 21 days, in result, splenic Band T lymphocytes, especially T/sub H/ lymphocytes were significantly increased compared with normal control group, and thymic T/sub H/ lymphocytes were also increased in WDCWT administrated group for 14 days. The results suggest that WDCWT extract inhibit a gastric acid secretion in mice stomach, and is useful in the treatment of the hyperacidity and gastric ulcer.
ANXA2, a member of the annexin family, is overexpressed and plays important roles in tumor development. However, the significance of ANXA2 expression in gastric carcinoma has not been clarified.To elucidate its roles in growth of gastric cancer, ANXA2 expression in SGC-7901 cells was inhibited with a designated siRNA, then cell proliferation, cell cycling, apoptosis and motility were determined by MTT assay, flow cytometry, Hoechst 33342 staining and wound healing assay, respectively. To further assess the behavior of ANXA2 deleted SGC-7901 cells, changes of microstructures were observed under fluorescence microscopy, laser scanning confocal microscopy and electron microscopy. We found that inhibition of ANXA2 expression caused cell proliferation to decrease significantly with G1 arrest, motility to be reduced with changes in pseudopodia/filopodia structure and F-actin and ${\beta}$-tubulin expression, and apoptosis to be enhanced albeit without significance. At the same time, ANXA2 deletion resulted in fewer pseudopodia/filopodia, non-stained areas were increased, contact inhibition among cells reappeared, and expression of F-actin and ${\beta}$-tubulin was decreased, with induction of polymerized disassembled forms. Taken together, these data suggest that ANXA2 overexpression is important to maintain the malignancy of cancer cells, and this member of the annexin family has potential to be considered as a target for the gene therapy of gastric carcinoma.
Kim, Dae-Yeon;Gweon, Bo-Mi;Kim, Dan-Bee;Choe, Won-Ho;Shin, Jennifer H.
Proceedings of the KSME Conference
/
2008.11a
/
pp.1539-1542
/
2008
Plasma is 4th state of matters, which consists of electrons, neutral, and ionized particles. In biomedical research, cold plasma, which is generated in atmospheric condition, has been applied to disinfect microorganisms such as bacteria and yeast cells. Because of its low temperature condition, the heat-sensitive medical device can be easily sterilized by the cold plasma treatment. In recent years, the effects of plasma on mammalian cells have arisen as a new issue. Generally, plasma induces intensity dependent necrotic cell death. In this research, we investigate the feasibility of cold plasma treatment for cancer therapy by conducting comparative study of plasma effects on normal and cancer cells. We use THLE-2 (human liver normal cell) and SK-Hep1 (human liver metathetic cancer cell) as our target cells. The needle type of cold plasma is generated by the Helium plasma device. Two types of cells have different onset plasma conditions for the necrosis, which may be explained by difference in electrical properties of these two cell types.
Kim, Sung-Hyum;Park, Wan-Su;Seong, Nak-Sull;Lee, Young-Jong
The Korea Journal of Herbology
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v.22
no.4
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pp.169-176
/
2007
Objective : This study purposed to investigate the anti-oxidative effect of Lithospermi Radix (root of Lithospermum erythrorhizon S.) on liver cells isolated from oxidatvely stressed rat by AAPH. Method : We investigate effects of Lithospermi Radix(LR) and its fractions on normal liver cells' proliferation. And the amounts of SOD, GSH, catalase, NO, MDA production by liver cells isolated from the oxidatively stressed rat by AAPH also were measured after incubation with various fractions of LR extraction. Results : LR and its fracitons showed no toxicity on the normal liver cells from rat. LR and its fracitons increased the activity of SOD and reduced the amounts of NO and MDA in the liver cells from the oxidatively stressed rat. Conclusion : Lithospermi Radix could be supposed to have antioxidant effect on liver cells with no toxicity.
Daynes, Raymond A.;Chung, Hun-Taeg;Roberts, Lee K.
The Journal of the Korean Society for Microbiology
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v.21
no.3
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pp.311-329
/
1986
The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.
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