Journal of Pathology and Translational Medicine

Original Articles

The Effect of Ginseng Saponin on the Dopaminergic Neurons in the Parkinson's Disease Model in Mice.: Chang Ok Kim, Ki Sok Kim, Young Buhm Huh, Byeong Woo Ahn, Beom Seok Han, Kwang Sik Choi, Ki Yul Nam, Sang Woo Juhng; Korean J Pathol. 1997;31(9):805-814.

Abstract PDF: Saponin has been known to be a major antioxidant component in panax ginseng. Recent experimental study suggests that some antioxidant materials prevent Parkinson's disease caused by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) in an animal model. The present study was performed to demonstrate the effect of ginseng saponins in the Parkinson's disease model induced by MPTP. To verify the effect of ginseng saponin on dopaminergic neurons in the mice brain, the tyrosine hydroxylase-immunoreactive (TH-ir) neurons were observed by immunohistochemical stain and immunoelectron microscopy (preembedding method). Also, in order to estimate the immunoreactivity of dopaminergic neuropils, they were quantified by image analysis. The number of TH-ir neurons of substantia nigra was significantly increased in the high-dose (0.46 mg/kg) ginseng saponin group compared with the MPTP injected group. The immunoreactivity of TH-ir neuropils in striatum was significantly increased in both high and low-dose (0.1 mg/kg) ginseng saponin groups compared with the MPTP injected group. In immunoelectron microscopic observation, TH-ir neurons of the control and both ginseng saponin injected group showed normal nuclei and well preserved cytoplasmic organelles. In the MPTP injected group, dying dopaminergic neurons showed destroyed nuclei and cytoplasmic organelles. These results suggest that ginseng saponin has a protective effect on the Parkinson's disease model induced by MPTP.

Expression of Antigenic Surface Molecules of Pneumocystis Carinii by Immunoelectron Microscopic Examination.: Kun Young Kwon, Seung Che Cho, Sang Pyo Kim, Kwan Kyu Park, Eun Sook Chang; Korean J Pathol. 1998;32(6):393-403.

Abstract: This study was carried out to investigate the morphologic characteristics and localization of antigenic molecules of Pneumocystis carinii in experimentally induced P. carinii pneumonia in rats. After six weeks of administration of low protein diet and dexamethasone, Sprague-Dawley rats were sacrificed to submit lungs or bronchoalveolar lavage for the study. Monoclonal (092, 900, 902, and 904) and polyclonal (SP-D) antibodies were used for immunohistochemistry and immunoelectron microscopy (ITEM and ISEM). Immunohistochemically P. carinii organisms were well identified as clusters or separated forms in the alveolar spaces being frequently attached to the alveolar walls. Immunoelectron microscopically the adherences of gold particles were observed on the surface of all stages of the P. carinii. Occasionally positive immunogold labeling was observed in the cytoplasm of the trophozoites and on the pellicle of the intracystic bodies within the cysts. The monoclonal antibodies 092, 900, 902, and 904 reacted mainly with pellicles of P. carinii, whereas SP-D labeled on the pellicles, intracystic bodies, cytoplasms of the alveolar macrophages, and free floated surfactant material in the alveolar spaces. The immunogold particles were observed more diffusely and intensely in the cysts than in the trophozoites. These results indicate that antigen is mainly localized on the pellicles, and accumulated during development from the trophozoite to the cyst stages.

Apoptosis of Alveolar Cells in Pneumocystis Carinii Pneumonia: Application of Electron Microscopic Terminal Deoxynucleotidyl Transferase-Mediated dUTP-Biotin Nick End Labeling Method.: Kyu Hun Kang, Sang Pyo Kim, Kun Young Kwon; Korean J Pathol. 2001;35(6):496-505.

Abstract: BACKGROUND
Pneumocystis carinii (P. carinii) attaches to alveolar cells and causes injury to the epithelial cells by direct toxic effects or inhibition of epithelial growth and replication. Although respiratory cell damage or death is a common feature in P. carinii pneumonia, there has been little reports about expression of apoptosis of the lung tissue in the literatures.
METHODS
We examined expression of fibronectin and vitronectin in the interaction between P. carinii and alveolar cells, and in situ terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL) expression of apoptosis in the respiratory cells by immunohistochemistry and pre-embedding immunoelectron microscopy.
RESULTS
Light microscopic (LM) and electron microscopic (EM) immunohistochemical stains for the fibronectin and vitronectin showed strong expressions on the pellicles and tubular extensions of P. carinii and weak expression along the surfaces of type I alveolar cells. LM and EM TUNEL stains showed positive expression in the nuclei of alveolar cells, apoptotic bodies in the cytoplasm of alveolar macrophages and cellular debris in alveolar spaces.
CONCLUSIONS
P. carinii induces injury and apoptosis of alveolar cells after attachment of the organisms to host cells, and alveolar macrophages enhance the clearance of apoptotic bodies of alveolar cells as well as phagocytosis and degradation of P. carinii.

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