• 제목/요약/키워드: ABCB1

검색결과 24건 처리시간 0.018초

카드뮴이 해양 섬모충(Euplotes crassus)의 ABC Transporters와 GST 유전자 발현에 미치는 영향에 관한 연구 (Effect of Cadmium on the Expression of ABC Transporters and Glutathione S-transferase in the Marine Ciliate Euplotes crassus)

  • 김호균;김세훈;김지수;이영미
    • 한국해양생명과학회지
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    • 제1권2호
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    • pp.79-87
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    • 2016
  • 카드뮴과 같은 중금속은 독성이 높아 수서 생물과 인간에게 해로운 영향을 미친다고 알려져 있다. 본 연구에서는 해양 섬모충 Euplotes crassus에서 카드뮴이 해독 기전에 관여하는 ABC transporters (ABCs)와 glutathione S-transferase (GST)의 유전자 발현에 미치는 영향을 조사하였다. 총 7개의 ABCs 유전자와 1개의 GST 유전자 일부를 클로닝하여 유전자 분석을 실시하였고, 카드뮴(0.1~1 mg/l) 노출에 따른 이들 유전자의 발현 양상을 quantitative real time RT-PCR (qRT-PCR)을 이용하여 분석하였다. 염기서열 분석과 계통 분석 결과 이들 ABCs 유전자가 ABC transporter의 특징을 가지며, ABC-B/C family에 속하는 것을 확인하였고, GST 유전자는 theta isoform과 유사한 것으로 나타났다. 카드뮴에 8시간 노출시킨 결과 ABC transporter 유전자의 경우 ABCB21 유전자를 제외하고는 대부분 농도 의존적으로 유전자 발현이 유의하게 증가하였다. GST 유전자는 0.5 mg/l에서 가장 높은 유전자 발현 양상을 보였으며, 1 mg/l에서는 발현량이 대조군 수준으로 감소되었다. 본 연구 결과는 E. crassus의 ABC transporter와 GST 유전자가 카드뮴에 의해 유도되는 독성에 대한 방어 기전에 참여하는 것을 의미한다.

벌사상자의 위염 치료 적용에 대한 네트워크 약리학적 분석 (Network Pharmacological Analysis of Cnidii Fructus Treatment for Gastritis)

  • 김영식;이승호
    • 동의생리병리학회지
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    • 제38권1호
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    • pp.22-26
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    • 2024
  • The purpose of this study was to identify the applicability, main compounds, and target genes of Cnidii Fructus (CF) in the treatment of gastritis using network pharmacology. The compounds in CF were searched in Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and a database of medicinal materials and chemical compounds in Northeast Asian traditional medicine (TM-MC). The target gene information of the compounds was collected from pubchem and cross-compared with the gastritis-related target gene information collected from Genecard to derive the target genes. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on the derived target genes. Afterwards, network analysis between compounds and disease target genes was performed using cytoscape. We identified 121 active compounds and 139 target genes associated with gastritis. Pathways derived from the GO biological process and KEGG pathway DB primarily focus on target genes related to inflammation (IL-6, IL-8, TNF production, NF-κB transcription factor activity, and NF-κB signaling pathway) and cell death (PI3K-Akt, FoxO). Major targets for CF treatment of gastritis include TP53, TNF, BCL2, EGFR, NFKB1, ABCB1, PPARG, PTGS2, IL6, IL1B, and SOD1, along with major compounds such as coumarin, osthol, hexadecanoic acid, oleic acid, linoleic acid, and stigmasterol. This study provided CF's applicability for gastritis, related compounds, and target information. Evaluating CF's effectiveness in a preclinical gastritis model suggests its potential use in clinical practice for digestive system diseases.

Transcriptome sequencing revealed the inhibitory mechanism of ketoconazole on clinical Microsporum canis

  • Wang, Mingyang;Zhao, Yan;Cao, Lingfang;Luo, Silong;Ni, Binyan;Zhang, Yi;Chen, Zeliang
    • Journal of Veterinary Science
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    • 제22권1호
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    • pp.4.1-4.13
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    • 2021
  • Background: Microsporum canis is a zoonotic disease that can cause dermatophytosis in animals and humans. Objectives: In clinical practice, ketoconazole (KTZ) and other imidazole drugs are commonly used to treat M. canis infection, but its molecular mechanism is not completely understood. The antifungal mechanism of KTZ needs to be studied in detail. Methods: In this study, one strain of fungi was isolated from a canine suffering with clinical dermatosis and confirmed as M. canis by morphological observation and sequencing analysis. The clinically isolated M. canis was treated with KTZ and transcriptome sequencing was performed to identify differentially expressed genes in M. canis exposed to KTZ compared with those unexposed thereto. Results: At half-inhibitory concentration (½MIC), compared with the control group, 453 genes were significantly up-regulated and 326 genes were significantly down-regulated (p < 0.05). Quantitative reverse transcription polymerase chain reaction analysis verified the transcriptome results of RNA sequencing. Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that the 3 pathways of RNA polymerase, steroid biosynthesis, and ribosome biogenesis in eukaryotes are closely related to the antifungal mechanism of KTZ. Conclusions: The results indicated that KTZ may change cell membrane permeability, destroy the cell wall, and inhibit mitosis and transcriptional regulation through CYP51, SQL, ERG6, ATM, ABCB1, SC, KER33, RPA1, and RNP genes in the 3 pathways. This study provides a new theoretical basis for the effective control of M. canis infection and the effect of KTZ on fungi.

Reversal of Multidrug Resistance and Computational Studies of Pistagremic Acid Isolated from Pistacia integerrima

  • Rauf, Abdur;Uddin, Ghias;Raza, Muslim;Ahmad, Aftab;Jehan, Noor;Ahmad, Bashir;Nisar, Muhammad;Molnar, Joseph;Csonka, Akos;Szabo, Diana;Khan, Ajmal;Farooq, Umar;Noor, Mah
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권4호
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    • pp.2311-2314
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    • 2016
  • Pistagremic acid (PA) is a bioactive triterpenoid isolated from various parts of Pistacia integerrima plants. The aim of this research was to investigate PA for reversion of multidrug resistant (MDR) mediated by P-glycoprotein using rhodamine-123 exclusion study on a multidrug resistant human ABCB1 (ATP-binding cassette, sub-family B, member 1) gene-transfected mouse T-lymphoma cell line in vitro. Results were similar to those with verapamil as a positive control. Docking studies of PA and standard Rhodamine123 were carried out against a P-gp crystal structure which showed satisfactory results. Actually, PA cannot bind exactly where co-crystallized ligand of P-gp is already present. However, the docking study predicted that if a compound gives a lesser score then it may have some potency. The docking scores of PA and Rhodamine were similar. Therefore, we can conclude that there are certain important chemical features of PA which are responsible for the inhibiting potency of P-gp.