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Inhibition of Tyrosine Hydroxylase by (1R,9S)-β-Hydrastine Hydrochloride in PC12 Cells
Shou Yu Yin,Yu Mi Kim,Jae Joon Lee,Chun Mei Jin,Yoo Jung Yang,Kyo Whan Lim,Min Hee Kang,Myung Koo Lee 한국생약학회 2004 Natural Product Sciences Vol.10 No.3
It is reported that (1R,9S)-b-hydrastine hydrochloride (BHSH) decreased the intracellular dopamine content by inhibiting tyrosine hydroxylase (TH) activity in PC12 cells. In this study, the inhibitory mechanisms on TH activity by BHSH in PC12 cells were investigated. BHSH treatment caused a reduction of TH activity and TH mRNA level in a dose-dependent manner. After the treatment of 20 mM BHSH, TH activity and TH mRNA content were reduced at 15 min, reached the minimal levels at 6-24 h, and then recovered gradually to the control level. BHSH at 10-50 mM caused a decrease in the basal intracellular cyclic AMP levels at 10 min in a concentration-dependent manner. In addition, BHSH at 20-100 mM decreased the basal intracellular Ca2+ concentration ([Ca2+]i) immediately in a dose-dependent manner. BHSH also inhibited the 56 mM K+ depolarization-induced elevation in [Ca2+]i, and blocked caffeine-activated store-operated Ca2+ entry in PC12 cells. These data suggest that BHSH inhibits TH activity and TH gene expression, in part, through reducing cyclic AMP content and basal [Ca2+]i in PC12 cells.
Shou Yu Yin,Jae Joon Lee,Yu Mi Kim,Chun Mei Jin,Yoo Jung Yang,Min Hee Kang,Myung Koo Lee 한국생약학회 2004 Natural Product Sciences Vol.10 No.3
The effects of BHSH on L-DOPA-induced increase in dopamine content in PC12 cells were investigated. L-DOPA treatment at 20 or 50 mM increased dopamine content after both 24 and 48 h of incubation in PC12 cells. However, the co-treatments of BHSH (10-50 mM) with L-DOPA (20 or 50 mM) significantly inhibited the increase of dopamine content induced by L-DOPA. BHSH treatment at 10-50 mM significantly inhibited basal aromatic L-amino acid decarboxylase (AADC) activity in a concentration-dependent manner at 15 min, and then AADC activity was rapidly recovered to the control level at about 2 h. These results indicate that the inhibition of AADC activity by BHSH was, in part, contributed to the early-stage decrease of dopamine content induced by LDOPA in PC12 cells. Taken together, it is proposed that the short-term inhibition of dopamine biosynthesis by BHSH was mediated by the regulation of tyrosine hydroxylace (TH).
Inhibitory Effects of (1R,9S)-β-Hydrastine on Calcium Transport in PC12 Cells
Shou Yu Yin,Chun Mei Jin,Yoo Jung Yang,Sung Cil Lim,이종길,황방연,Jai Seup Ro,이명구 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.1
(1R,9S)-β-Hydrastine (BHS), at 100 μM, has been shown to mainly reduce the K+-induced dopamine release and Ca2+ influx by blocking the L-type Ca2+ channel and inhibit the caffeine activated store-operated Ca2+ channels, but not those activated by thapsigargin, in PC12 cells. In this study, the effects of BHS on Ca2+ transport from Ca2+ stores in the absence of external Ca2+ were investigated in PC12 cells. BHS decreased the basal intracellular Ca2+ concentration ([Ca2+]i) in the absence of external Ca2+ in PC12 cells. In the absence of external Ca2+, pretreating PC12 cells with 100 μM BHS reduced the rapid increase in the [Ca2+]i elicited by 20 mM caffeine, but not that by 1 μM thapsigargin. In addition, BHS inhibited the increase in the [Ca2+]i elicited by restoration of 2 mM CaCl2 after the Ca2+ stores had been depleted by 20 mM caffeine, but not those depleted by 1 μM thapsigargin, in the absence of external Ca2+. These results suggested that BHS mainly inhibited Ca2+ leakage from the Ca2+ stores and the caffeine- stimulated release of Ca2+ from the caffeine-sensitive Ca2+ stores in PC12 cells.
Inhibitory Effects of $(1R,9S)-{\beta}-Hydrastine$ on Calcium Transport in PC12 Cells
Yin, Shou Yu,Jin, Chun-Mei,Yang, Yoo-Jung,Lim, Sung-Cil,Lee, Chong-Kil,Hwang, Bang-Yeon,Ro, Jai-Seup,Lee, Myung-Koo 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.1
[ $(1R,9S)-{\beta} ]-Hydrastine$ (BHS), at $100{\mu}M$, has been shown to mainly reduce the $K^+-induced$ dopamine release and $Ca^{2+}$ influx by blocking the L-type $Ca^{2+}$ channel and inhibit the caffeine activated store-operated $Ca^{2+}$ channels, but not those activated by thapsigargin, in PC12 cells. In this study, the effects of BHS on $Ca^{2+}$ transport from $Ca^{2+}$ stores in the absence of external $Ca^{2+}$ were investigated in PC12 cells. BHS decreased the basal intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in the absence of external $Ca^{2+}$ in PC12 cells. In the absence of external $Ca^{2+}$, pre-treating PC12 cells with $100{\mu}M$ BHS reduced the rapid increase in the $[Ca^{2+}]_i$ elicited by 20mM caffeine, but not that by $1{\mu}M$ thapsigargin. In addition, BHS inhibited the increase in the $[Ca^{2+}]_i$ elicited by restoration of 2mM $CaCl_2$ after the $Ca^{2+}$ stores had been depleted by 20mM caffeine, but not those depleted by $1{\mu}M$ thapsigargin, in the absence of external $Ca^{2+}$. These results suggested that BHS mainly inhibited $Ca^{2+}$ leakage from the $Ca^{2+}$ stores and the caffeine-stimulated release of $Ca^{2+}$ from the caffeine-sensitive $Ca^{2+}$ stores in PC12 cells.
Effects of (1R,9S)-β-Hydrastine Hydrochloride on L-DOPA-Induced Cytotoxicity in PC12 Cells
Shou Yu Yin,Jae Joon Lee,Yu Mi Kim,Chun Mei Jin,Yoo Jung Yang,Myung Koo Lee 한국생약학회 2004 Natural Product Sciences Vol.10 No.3
Previously, (1R,9S)-b-hydrastine hydrochloride has been found to lower dopamine content in PC12 cells (Kim et al., 20001). In this study, the effects of (1R,9S)-b-hydrastine hydrochloride on L-DOPA-induced cytotoxicity in PC12 cells were investigated. Treatment with (1R,9S)-b-hydrastine hydrochloride at concentrations higher than 500 mM caused cytotoxicity in PC12 cells. In addition, (1R,9S)-b-hydrastine hydrochloride at non-cytotoxic or cytotoxic concentrations significantly enhanced L-DOPA-induced cytotoxicity (L-DOPA concentration, 50 μM). Treatment of PC12 cells with 750 μM 1R,9S)-b-hydrastine hydrochloride and 50 μM L-DOPA, alone or in combination, also induced cell death via a mechanism which exhibited morphological and biochemical characteristics of apoptosis, including chromatin condensation and membrane blebbing. Exposure of PC12 cells to (1R,9S)-b- hydrastine hydrochloride, L-DOPA and (1R,9S)-b-hydrastine hydrochloride plus L-DOPA for 48 h resulted in a marked increase in the cell loss and percentage of apoptotic cells compared with exposure for 24 h. These data indicate that (1R,9S)-b-hydrastine hydrochloride at higher concentration ranges aggravates L-DOPA-induced neurotoxicity cytotoxicity in PC12 cells. Therefore, it is proposed that the long-term L-DOPA therapeutic patients with (1R,9S)-b-hydrastine hydrochloride could be checked for the adverse symptoms.
Inhibition of Calcium Transport by (1R,9S)-β-HydrastineHydrochloride in PC12 Cells
Shou Yu Yin,이명구 한국생약학회 2006 Natural Product Sciences Vol.12 No.4
effects of (1R,9S)-β2+ transport in rat pheochromo-cytoma PC12 cells were investigated. In the presence of external Ca2+, BHSH at 100M inhibited K+ (56 mM)-induced dopamine release, and K+-induced Ca2+ influx and a sustained rise of [Ca2+]i. In addition, BHSH at100 M reduced the sustained rise of [Ca2+]i elicited by 20 mM cafeine, but not by 1M thapsigargin, inpresence of external Ca2+. These results suggest that BHSH inhibited K+-induced dopamine release and [Ca2+]iinflux, and store-operated Ca2+ channels activated by cafeine, but not by thapsigargin, in PC12 cells. Keywords(1R,9S)-β-Hydrastine hydrochloride, K+-induced dopamine release, caffeine-stimulated Ca2+ release,store-operated Ca2+ channel, PC12 cells
Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
Jiang, Dao-Jun,Yu, Hong-Xiu,Hexige, Sa-Yin,Guo, Ze-Kun,Wang, Xiang,Ma, Li-Jie,Chen, Zheng,Zhao, Shou-Yuan,Yu, Long Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCP10L in human hepatocarcinomas.
Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
( Dao Jun Jiang ),( Hong Xiu Yu ),( Sa Yin Hexige ),( Ze Kun Guo ),( Xiang Wang ),( Li Jie Ma ),( Zheng Chen ),( Shou Yuan Zhao ),( Long Yu ) 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCPIOL in human hepatocarcinomas.
Zhou, Wen-xiu,Hou, Wen-bo,Zhou, Chao,Yin, Yu-xia,Lu, Shou-tao,Liu, Guang,Fang, Yi,Li, Jian-wen,Wang, Yan,Liu, Ai-hua,Zhang, Hai-jun The Korean Neurosurgical Society 2021 Journal of Korean neurosurgical society Vol.64 No.2
Objective : Shunt infection is a common complication while treating hydrocephalus. The antibiotic-impregnated shunt catheter (AISC) was designed to reduce shunt infection rate. A meta-analysis was conducted to study the effectiveness of AISCs in reduction of shunt infection in terms of age, follow-up time and high-risk patient population. Methods : This study reviewed literature from three databases including PubMed, EMBASE, and Cochrane Library (from 2000 to March 2019). Clinical studies from controlled trials for shunt operation were included in this analysis. A subgroup analysis was performed based on the patient's age, follow-up time and high-risk population. The fixed effect in RevMan 5.3 software (Cochrane Collaboration) was used for this meta-analysis. Results : This study included 19 controlled clinical trials including 10105 operations. The analysis demonstrated that AISC could reduce the infection rate in shunt surgery compared to standard shunt catheter (non-AISC) from 8.13% to 4.09% (odds ratio [OR], 0.48; 95% confidence interval [CI], 0.40-0.58; p=0.01; I2=46%). Subgroup analysis of different age groups showed that AISC had significant antimicrobial effects in all three groups (adult, infant, and adolescent). Follow-up time analysis showed that AISC was effective in preventing early shunt infections (within 6 months after implant). AISC is more effective in high-risk population (OR, 0.24;95% CI, 0.14-0.40; p=0.60; I2=0%) than in general patient population. Conclusion : The results of meta-analysis indicated that AISC is an effective method for reducing shunt infection. We recommend that AISC should be considered for use in infants and high-risk groups. For adult patients, the choice for AISC could be determined based on the treatment cost.