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Institute for Advanced Research in Asian Science a 2010 The American journal of Chinese medicine Vol.38 No.4
<P>EGb 761 is an extract of Gingko biloba that exhibits neuroprotective effects against cerebral ischemia. The mammalian target of rapamycin (mTOR) is a critical downstream effector of Akt and a central regulator of ribosomal biogenesis and protein synthesis. We investigated whether EGb 761 regulates Akt downstream targets, including mTOR, p70S6 kinase, and S6 phosphorylation. Adult male rats were treated with vehicle or EGb 761 (100 mg/kg) prior to middle cerebral artery occlusion (MCAO). Brains were collected at 24 hours after MCAO and the cerebral cortex regions were examined. We previously showed that EGb 761 significantly reduces infarct volume and decreases the number of TUNEL-positive cells in the cerebral cortex. Ischemic brain injury induces a decrease in Akt up-stream target, PDK1 phosphorylation. The levels of phospho-mTOR, phospho-p70S6 kinase, and phospho-S6 are subsequently decreased in regions affected by ischemic injury. However, EGb 761 prevented injury-induced decreases in these protein levels. We confirmed that EGb 761 inhibits injury-induced decreases in the number of positive cells for phospho-p70S6 kinase and phospho-S6. The results of this study provide evidence that EGb 761 protects neuronal cells against ischemic brain injury by preventing injury-induced decreases in p70S6 kinase and S6 phosphorylation.</P>
Expression of placenta growth factor mRNA in the rat placenta during mid-late pregnancy
Phil-Ok Koh,Wan-Sung Choi,Gyeong-Jae Cho,Chung-Kil Won 대한수의학회 2005 Journal of Veterinary Science Vol.6 No.3
The placenta is an essential organ that synthesizes several growth and angiogenic factors for its own growth as well as fetal development. It is known that the placenta growth factor (PlGF) is a member of the vascular endothelial growth factor family and is critical for placental growth and fetal development. However, there is little information regarding the expression pattern and cellular localization of PlGF mRNA in rat placenta during pregnancy. The aim of this study was to define the distribution of PlGF mRNA in rat placenta at various gestations. RT-PCR analysis showed that the expression level of PlGF mRNA increased as gestation advanced. Using in situ hybridization histochemistry, positive cells of PlGF mRNA were detected in chorionic villi. PlGF mRNA was expressed in the trophoblast cells and stroma cells surrounding the blood vessels within chorionic villi on day 13 and 15. Also, positive signals of PlGF mRNA were strongly detected in stroma cells of chorionic villi on day 17, 19, and 21. In particular, the density and number of positive signals of PlGF mRNA was significantly increased as gestation advanced. The expression pattern of PlGF mRNA in rat placenta during pregnancy demonstrates that PlGF plays a functional role for placental growth and fetal development during mid-late pregnancy.
Phil-Ok Koh 한국실험동물학회 2010 Laboratory Animal Research Vol.26 No.3
PEA-15 is a small phosphoprotein (15 kDa) that is enriched in brain astrocytes. PEA-15 acts as an important modulator of cellular function including apoptosis and signal integration. This study investigated the expression of PEA-15 in focal cerebral ischemic injury. Cerebral ischemia was surgically induced in adult male rats by middle cerebral artery occlusion (MCAO), and brains were collected 24 hr after MCAO. A proteomic approach demonstrated decreases of PEA-15 protein spots in MCAO-operated animals in comparison to sham-operated animals. Western blot analysis clearly demonstrated that MCAO induces decreases in PEA-15 levels. We previously showed that glutamate toxicity induces cell death in a hippocampus-derived cell line (HT22). Glutamate exposure induces decreases of PEA-15 levels in HT22 cells. The results of this study suggest that focal cerebral ischemia induces cell death through downregulation of PEA-15 protein.
Estradiol Increases Heme Oxygenase-1 Expression in Brain Ischemic Injury
Phil-Ok Koh 한국실험동물학회 2006 Laboratory Animal Research Vol.22 No.2
This study investigated whether estradiol modulates the heme oxygenase-1 (HO-1) and HO-2 expressions in brain ischemic injury. Adult female rats were ovariectomied and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 h after MCAO and infarct volumes were analyzed. Estradiol administration significant-reduced infarct volume and decreased the positive cells of TUNEL staining in the cerebral cortex. Activation of HO-1 and HO-2 was measured using Western blot analysis. Estradiol increased the level of HO-1 in ischemic injury induced by MCAO. The level of HO-1 was 0.81 ± 0.15 and 0.97 ± 0.25 in the ipsilateral cortex of oil-and estradiol-treated animals, respectively. However, the level of HO-2 was consistently maintained in the ipsilateral cortex of oil- and estradiol-treated animals. Our findings suggest that estradiol prevents cell death caused by neuronal cell injury through the increase of HO-1 expression.
Nicotinamide restores the reduction of parvalbumin in cerebral ischemic injury.
The Society ; Maruzen Co. [distributor] 2013 The Journal of veterinary medical science Vol.75 No.2
<P>The aim of this study investigated whether nicotinamide affects parvalbumin expression in focal cerebral ischemic injury. Rats were treated with vehicle or nicotinamide (500 mg/kg) 2 hr after middle cerebral artery occlusion (MCAO), and cerebral cortex tissues were collected 24 hr after MCAO. Nicotinamide significantly decreases the volume of infarct areas in the cerebral cortex. A proteomic approach revealed that MCAO induces decreases of parvalbumin levels, while nicotinamide treatment prevents injury-induced decreases in parvalbumin. RT-PCR and Western blot analyses demonstrated that nicotinamide restores injury-induced decreases in parvalbumin. Moreover, immunohistochemical staining confirmed that the numbers of parvalbumin-positive cells were decreased in vehicle-treated animals with MCAO, and that nicotinamide averted this decrease. In cultured hippocampal cells, nicotinamide treatment prevents the glutamate exposure-induced increase in intracellular Ca(2+) concentration and decrease in parvalbumin expression. These results suggest the fact that the maintenance of parvalbumin expression is mediated to the neuroprotective function of nicotinamide against ischemic brain injury.</P>
Ethanol Exposure Decreases Cell Proliferation and Increases Apoptosis in Rat Testes
KOH, Phil-Ok,KIM, Myeong-Ok Japanese Society of Veterinary Science 2006 The Journal of veterinary medical science Vol.68 No.10
<P>Ethanol exposure is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether chronic ethanol exposure decreases proliferative activity or increases apoptosis in the testes. Ethanol (1.5 g/kg or 3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Proliferating cell nuclear antigen (PCNA) was used as a proliferative marker. Western blot analysis showed that ethanol administration significantly reduced the level of PCNA. Also, immunoreactivity of PCNA-positive cells in the spermatogonia and primary spermatocytes were decreased by ethanol exposure. However, the number of TUNEL-positive cells was significantly increased in the testicular germ cells of ethanol-treated rats. Moreover, ethanol administration significantly increased the level of activated caspase-3 in testes. In conclusion, our findings suggest that ethanol may partly contribute to the suppression of male reproductive activity through a reduction of cell proliferation and an enhancement of cell death in rat testes.</P>