The effect of Bu-Zhong-Yi-Qi-Tan (BZYQT) on the changes of ultraviolet (UV) light B radiation-induced apoptotic sunburn cell (SBC) and epidermal ATPase-positive dendritic cell (DC) in SKH1-hr or ICR mouse were investigated. The mice were treated with UVB (200 mj/㎠) and were sacrificed 24 h later. BZYQT (50 mg/kg of body weight) or vehicle (saline) was given i.p. at 36 and 12 h before irradiation, and 30 min after irradiation or BZYQT cream (0.2%) or cream base (vehicle) was topically treated at 24 h and 15 min before irradiation, and immediately after irradiation. The skin of SKH1-hr mouse prepared from the back of untreated mice exhibited about 0.3 SBC/cm length of epidermis, and 24 h after UV irradiation, the applied areas show an increased number of SBCs. But the frequency of UVB-induced SBC formation was reduced by intraperitoneal injection of BZYQT extract (p less than 0.01). The numbers of DC in normal ICR mouse were 628.00 ± 51.56 or 663.20 ± 62.58 per ㎟ of ear epidermis. By 1 day after UVB treatment, the number of ATPase-positive cells/㎟ were decreased by 39.0% or 27.1% in i.p. or topical application group with vehicle. Treatment of BZYQT was associated with increase of 33.9% in i.p. group (p less than 0.05) or 2.7% in topical application group in the number of ATPase positive cells compared with the irradiation control group. The results presented herein that BZYQT administration could reduce the extent of skin damages produced by UVB.

Ontogeny, distributions and relative frequencies of somatostatin-immunoreactive cells were investigated in the proventriculus of the chicken embryos with incubation periods. Samples were taken from 10 groups(10 days of incubation to hatching) and studied by immunogistochemical methods. The findings were as follows. Somatostatin-immunoreactive cells were observed from 12 days of incubation in the proventricular glands and after that increased with incubation periods. The first observation time of these cells in the epithelium were at 15 days of incubation in the basal portion but in 16 and 17 days of incubation, no immunoreactive cells were observed in the epithelium but after that a few immunoreactive cells were observed in the basal portion and gastric gland regions. The shpaes of these cells were spherical to spindle in the proventricular glands and spherical to round in the epithlium and gastric gland.

Glatiramer acetate (GA; Copaxone) has been shown to be effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). It has been recently shown that GA-reactive T cells migrate through the blood-brain barrier, accumulate in the central nervous system (CNS), secrete antiinflammatory cytokines and suppress production of proinflammatory cytokines of EAE and MS. Development of EAE requires coordinated expression of a number of genes involved in the activation and effector functions of inflammatory cells. Activation of inflammatory cells is regulated at the transcriptional level by several families of transcription factors. One of these is the nuclear factor kappa B (NFκB) family which is present in a variety of cell types and involved in the activation of immune-relative genes during inflammatory process. Since it is highly activated at site of inflammation, NFκB activation is also implicated in the pathogenesis of EAE. In this study, we examined whether the inhibition of NFκB activation induced by GA can have suppressive therapeutic effects in EAE mice. We observed the expression of NFκB and phospho-IκB proteins increased in GA-treated EAE mice compared to EAE control groups. The immunoreactivity in inflammatory cells and glial cells of NFκB and phospho-IκB significantly decreased at the GA-treated EAE mice. These results suggest that treatment of GA in EAE inhibits the activation of NFκB and phophorylation of IκB in the CNS. Subsequently, the inhibition of NFκB activation and IκB phosphorylation leads to the anti-inflammatory effects thereby to reduce the progression and severity of EAE.

Human granulocytic anaplasmosis (HGA) is caused by the obligate intracellular bacterium Anaplasma (A.) phagocytophilm. Natural killer T (NKT) cells are key players in host defense against various microbial infections. We investigated the role of NKT cells in immune response to A. phagocytophilum infection using NKT-knockout (Jα18-/-) mice. Jα18-/- and wild-type (WT) mice were infected with low-passage A. phagocytophilum and assayed for hepatic histopathology and cytokine production during 7 days post-infection. Compared to WT control, the infected Jα18-/- mice had much less histopathologic lesions and less apoptosis through day 7, and lower concentrations of IFN-γ and IL-12, but not of IL-10. This result suggests that NKT cells are major components in the pathogenesis of HGA.

The regional distributions and relative frequencies of the gastrin, secretin and pancreatic polypeptide(PP)-immunoreactive cells in the gastrointestinal tract of the fetus(180 days of gestation) of Korean native goat were sutdied with immunohistochemical(ABC) methods. Gastrin-immunoreactive cells were detected in fundus, pylorus and duodenum and these cells were most predominant in pylorus. Secretin-immunoreactive cells were observed in pylorus, duodenum and ileum. PP-immunoreactive cells were restricted to fundus. These immunoreactive cells were situated in surfact epithelium and mucosal gland regions. The regional distribution and relative frequency of PP-immunoreactive cells was somewhat different to the adult Korean native goat. Immunoreactive cells in thesurface epithelial regions were open typed cells which were spindle shaped cells but closed typed cells which were round or/to spherical shaped cells were observed in the mucosal gland regions.

The purposes of this study were to set up the method of the natural killer(NK) cell activity assay using the flow cytometer and to examine the characteristics and distribution of the NK cell during rat hepatocarcinogenesis. Forty five male 6 week-old specific pathogen free(SPF) Sprague-Dawley rats were randomly divided into three groups. Group I was the non-treated control and given normal diet and water. Group II was treated with diethylnitrosamine(DEN, 200mg/kg, i.p.) and partial hepatectomy. Group III was treated with DEN, partial hepatectomy and 0.05% phenobarbital sodium in water from 3 to 16 weeks. All animals were examined the morphology of the large granular lymphocyte(LGL), the LGL percent of the total lymphocytes and the LGL conjugation rate with YAC-1 cell in peripheral blood, spleen and liver. Moreover, activity of the LGL isolated from peripheral blood lymphocytes was determined using the flow cytometer. As results, LGL were observed in the peripheral blood, spleen and liver. LGL were observed the relatively faintly staining basophilic cytoplasm with granules, and eccentric, often kidney-shpaed nuclei in Giemsa stain. Its size was 11~13 micro meter. LGL percentage of the isolated lymphocytes in peripheral blood, spleen and liver were 1.8~2.3%, 1.3~1.4% and 0.87~0.99%, respectively. LGL conjugation rate with YAC-1 cell was shown to be peripheral blood(9.3~10.3%) spleen(7.7%~8.7%)liver(5.6~7.0%). The activity of the LGL isolated from peripheral blood lymphocytes in Group I, II and III was 33.7%, 30.5% and 35.4%, respectively. However, all values were not sighificantly between groups.

The regional distributions and relative frequencies of the gastrointestinal endocrine cells inthe gean goose (Anser fabalisLatham) were investigated by immunohistochemical methods using bovineSp-1/chromogranin (CG), serotonin, gastrin, cholecystokinin (CCK)-8, somatostatin and glucagon antisera. BCG-immunoreactive cells were widespread throughout the gastrointestinal tract (GIT) with moderated frequencies except for the gizzard and proventriculus which were a few frequencies. Serotonin-immunoreactive cells were detected throughout the GIT except for the proventriculus and gizzard. These cells wer observed inthe pylorus with rare frequencies but numerous cells wee cetected in the intestinal tract. Gastrin-immunoreactive cells were restricted to the gizzard, pylorus and duodenum. These cells were most predominant in the pylorus and a few or rare in the gizzard and duodenum, respectively. CCK-8-immunoreactive cells were observed from the gizzard to ileum. the highest frequencies of endocrine cells were observed in the duodenum. These cells were increased from the gizzard to duodenum but thereafter decreased. Somatostatin-immunoreactive cells were detected in the GIT except for the large intestine. In the proventriculus and pylorus, numerous immunoreactive cells were demonstrated but a few cells were present in the other regions. Glucagon cells were observed in the gizzard, pylorus, ileum, colon and rectum with a few or moderated numbers.

When an organism is exposed to various toxicants chronically, reactive oxygen species(ROS) are accumulated and eventually result in several biological effects from gene expression to cell death. In the present study we investigated the oxidative damage of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin(TCDD) and/or benzo(a)pyrene (B(a)P) in C100 cells. C100 cells treated with TCDD(30 nM) and B(a)P(3 μM) underwent diverse oxidative stress as determined through thiobarbituric acid-reactive substances(TBARS) formation, DNA fragmentation, DNA single strand break(SSB) assay, immunohistochemical staining of 8-hydroxy-2'-deoxyguanosine(8-OHdG), and mRNA expressions of antioxidant enzymatic genes such as Cu/Zn-SOD gene, GPx(glutathione peroxidase 5) gene, and catalase gene.

The ubiquitin-proteasome mediated protein degradation pathway plays an important role in regulating both cell proliferation and cell death. Proteasome inhibitors are well known to induce apoptosis in various human cancer cell lines. We investigated the effect of combined treatment with proteasome inhibitor and TRAIL, and a possible mechanism of the enhancing apoptosis by the both treatment, on TRAIL-resistant non-small cell lung cancer. A549 cells were exposed to the N-Acetyl-Leu-Leu-Norleu-al(ALLN) as a proteasome inhibitor and then treated with recombinant TRAIL protein. In A 549 cells under proteasome inhibition conditions by pretreatment with ALLN, TRAIL treatment significantly decreased cell vibility compared to that ALLN and TRAIL alone treatment. Also, the both treatment induced cell damage through DNA fragmentation and p53 expression. In addition, the combined treatment of both markedly increased caspase-8 activation, especially the exposure for 2h, and Bax expression and induced the dissipation of mitochondrial transmembrane potential in A549 cells. Taken together, these findings showed that proteasome inhibition by ALLN enhanced TRAIL-induced apoptosis via DNA degradation by activated P53 and mitochondrial transmembrane potential loss by caspase-8 activation and bax expression. Therefore, our results suggest that proteasome inhibitor may be used a very effectively chemotherapeutic agent for the tumor treatment, especeally TRAIL-resistant tumor cell.

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.