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| 1 | Pretreated Glehnia littoralis Extract Prevents Neuronal Death Following Transient Global Cerebral Ischemia through Increases of Superoxide Dismutase 1 and Brain-derived Neurotrophic Factor Expressions in the Gerbil Hippocampal Cornu Ammonis 1 Area显示文摘 | Joon Ha Park Tae-Kveono Lee Bing-Chun Yan Bich-Na Shin Ji Hyeon Ahn In Hye Kim Jeong Hwi Cho Jae-Chul Lee In Koo Hwang Jong Dai Kim Seongkweon Hong Young Joo Lee Moo-Ho Woll Il Jun Kang | 2017 | Chinese Medical Journal2017，，15： | 10 |
| 2 | Ethanol extract of Oenanthe javanica increases cell proliferation and neuroblast differentiation in the adolescent rat dentate gyrus显示文摘Oenanthe javanica is an aquatic perennial herb that belongs to the Oenanthe genus in Apiaceae family, and it displays well-known medicinal properties such as protective effects against glutamate-induced neurotoxicity. However, few studies regarding effects of Oenanthe javanica on neurogenesis in the brain have been reported. In this study, we examined the effects of a normal diet and a diet containing ethanol extract of Oenanthe javanica on cell proliferation and neuroblast differentiation in the subgranular zone of the hippocampal dentate gyrus of adolescent rats using Ki-67(an endogenous marker for cell proliferation) and doublecortin(a marker for neuroblast). Our results showed that Oenanthe javanica extract significantly increased the number of Ki-67-immunoreactive cells and doublecortin-immunoreactive neuroblasts in the subgranular zone of the dentate gyrus in the adolescent rats. In addition, the immunoreactivity of brain-derived neurotrophic factor was significantly increased in the dentate gyrus of the Oenanthe javanica extract-treated group compared with the control group. However, we did not find that vascular endothelial growth factor expression was increased in the Oenanthe javanica extract-treated group compared with the control group. These results indicate that Oenanthe javanica extract improves cell proliferation and neuroblast differentiation by increasing brain-derived neurotrophic factor immunoreactivity in the rat dentate gyrus. | Bai Hui Chen Joon Ha Park Jeong Hwi Cho In Hye Kim Bich Na Shin Ji Hyeon Ahn Seok Joon Hwang Bing Chun Yan Hyun Jin Tae Jae Chul Lee Eun Joo Bae Yun Lyul Lee Jong Dai Kim Moo-Ho Won Il Jun Kang | 2015 | Neural Regeneration Research2015，10，2： | 1 |
| 3 | Decreased Insulin-Like Growth Factor-I and Its Receptor Expression in the Hippocampus and Somatosensory Cortex of the Aged Mouse显示文摘 | Choong Hyun Lee Ji Hyeon Ahn Joon Ha Park Bing Chun Yan In Hye Kim Dae Hwan Lee Jeong-Hwi Cho Bai Hui Chen Jae-Chul Lee Jun Hwi Cho Yun Lyul Lee Moo-Ho Won Il-Jun Kang | 2014 | Neurochemical Research2014，，4： | 1 |
| 4 | A nationwide seroepidemiology of hepatitis C virus infection in South Korea显示文摘 | Do Young Kim In Hee Kim Sook‐Hyang Jeong Yong Kyun Cho Joon Hyoek Lee Young‐Joo Jin Don Lee Dong Jin Suh Kwang‐Hyub Han Neung Hwa Park Ha Yan Kang Young Kul Jung Young Seok Kim Kyung‐Ah Kim Youn Jae Lee Byung Seok Lee Hyung Joon Yim Heon Ju Lee Soon Koo B | 2013 | Liver Int2013，，4： | 1 |
| 5 | Long-term treatment outcomes of clevudine in antiviral-naive patients with chronic hepatitis B显示文摘AIM:To evaluate the treatment outcomes of clevudine compared with entecavir in antiviral-naive patients with chronic hepatitis B(CHB).METHODS:We retrospectively analyzed the clinical data of CHB patients treated with clevudine 30 mg/d and compared their clinical outcomes with patients treated with entecavir 0.5 mg/d.The biochemical response,as assessed by serum alanine aminotransferase(ALT) activity,virologic response,as assessed by serum hepatitis B virus DNA(HBV DNA) titer,serologic response,as assessed by hepatitis B e antigen(HBeAg) status,and virologic breakthrough with genotypic mutations were assessed.RESULTS:Two-hundred and fifty-four patients [clevudine(n = 118) vs entecavir(n = 136)] were enrolled.In clevudine-treated patients,the cumulative rates of serum ALT normalization were 83.9% at week 48 and 91.5% at week 96(80.9% and 91.2% in the entecavir group,respectively),the mean titer changes in serum HBV DNA were-6.03 and-6.55 log 10 copies/mL(-6.35 and-6.86 log 10 copies/mL,respectively,in the entecavir group),and the cumulative non-detection rates of serum HBV DNA were 72.6% and 83.1%(74.4% and 83.8%,respectively,in the entecavir group).These results were similar to those of entecavir-treated patients.The cumulative rates of HBeAg seroconversion were 21.8% at week 48 and 25.0% at week 96 in patients treated with clevudine,which was similar to patients treated with entecavir(22.8% and 27.7%,respectively).The virologic breakthrough in the clevudine group occurred in 9(7.6%) patients at weeks 48 and 15(12.7%) patients at week 96,which primarily corresponded to genotypic mutations of rtM204I and/or rtL180M.There was no virologic breakthrough in the entecavir group.CONCLUSION:In antiviral-naive CHB patients,longterm treatment outcomes of clevudine were not inferior to those of entecavir,except for virologic breakthrough. | Suk Bae Kim Il Han Song Young Min Kim Ran Noh Ha Yan Kang Hyang Ie Lee Hyeon Yoong Yang An Na Kim Hee Bok Chae Sae Hwan Lee Hong Soo Kim Tae Hee Lee Young Woo Kang Eaum Seok Lee Seok Hyun Kim Byung Seok Lee Heon Young Lee | 2012 | World Journal of Gastroenterology2012，18，47： | 1 |
| 6 | Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death显示文摘Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperitoneal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen(Neu N; a neuronal marker) and Fluoro-Jade B(a marker for the localization of neuronal degeneration) was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67(a marker for proliferating cells)-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin(DCX; a marker for newly generated neurons)-immunoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2′-deoxyuridine(Brd U)-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature Brd U/Neu N double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death. | Bing Chun Yan Joon Ha Park Bai Hui Chen Jeong-Hwi Cho In Hye Kim Ji Hyeon Ahn Jae-Chul Lee In Koo Hwang Jun Hwi Cho Yun Lyul Lee Il-Jun Kang Moo-Ho Won | 2014 | Neural Regeneration Research2014，9，19： | 0 |
| 7 | Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions显示文摘To examine the effects of Populus tomentiglandulosa(PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1(CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia(TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg–1 PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor(BDNF) and insulin-like growth factor I(IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg–1 PT extract prevented neuronal death(loss). Furthermore, pretreatment with 200 mg·kg–1 PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI. | Tae-Kyeong Lee Joon Ha Park Ji Hyeon Ahn Hyunjung Kim Minah Song Jae-Chul Lee Jong Dai Kim Yong Hwan Jeon Jung Hoon Choi Choong Hyun Lee In Koo Hwang YAN Bing-Chun Moo-Ho Won Il Jun Kang | 2019 | Chinese Journal of Natural Medicines2019，17，6： | 0 |
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