RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제
      • 좁혀본 항목 보기순서

        • 원문유무
        • 원문제공처
        • 등재정보
        • 학술지명
        • 주제분류
        • 발행연도
        • 작성언어
        • 저자
          펼치기

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Characterization of LC3 and p62 on Rat Prostate Lobe in Benign Prostate Hyperplasia Animal Model

        Geum-Lan Hong,Kyung-Hyun Kim,Shanika Karunasagara,Ju-Young Jung 대한체질인류학회 2020 대한체질인류학회지 Vol.33 No.4

        Benign prostatic hyperplasia (BPH) is disease characterized by abnormal prostate cell proliferation. Rat models of testosterone propionate (TP)-induced BPH are the most popular experimental models for studying BPH. In rats, the prostate is located below the base of the urinary bladder and comprises four distinct lobes - ventral, lateral, dorsal, and anterior. Autophagy associated with cellular homeostasis has been studied in relation to BPH. Microtubule-associated proteins 1A/1B-light chain 3 (LC3B) and sequestosome 1 (p62) are key markers of autophagy flux. However, the expression and localization of LC3B and p62 have not been elucidated in rats with testosterone-induced BPH. This study investigated the expression and specific localization of the two autophagy markers mentioned. Fifteen Sprague-Dawley rats were classified into three groups: normal control (N.C.), BPH (TP 5 mg/kg), and Fina (TP+finasteride 10 mg/kg). To evaluate the expression of the autophagy markers in BPH, hematoxylin and eosin staining and immunohistochemistry were performed for LC3B and p62. Both LC3B expression and p62 expression were higher in the anterior lobe than other areas. In addition, there was no significant difference in the dorsal lobe LC3B expression among the N.C., BPH, and Fina groups. In the lateral lobe, LC3B expression was decreased in the BPH group and increased in the Fina group. p62 expression in the BPH and Fina groups increased compared to that in the N.C. group. In the ventral lobe of the prostate, LC3B expression was lower in the BPH group, whereas it was higher in the Fina group. On the other hand, p62 expression increased in the BPH group, whereas it was lower in the Fina group similar to those observed in the N.C. group. Autophagy was suppressed in the BPH group, whereas it was induced in the ventral lobe in the Fina group. Based on our finding, we suggest that autophagy is a critical process in BPH. In particular, the ventral lobe of the rat prostate could be a potential target site for evaluating the therapeutic effects of BPH treatment in animal models.

      • SCOPUSKCI등재

        Autophagy localization and cytoprotective role in cisplatin-induced acute kidney injury

        Karunasagara, Shanika,Hong, Geum-Lan,Jung, Da-Young,Ryu, Si-Yun,Jung, Ju-Young The Korean Society of Veterinary Science 2019 大韓獸醫學會誌 Vol.59 No.3

        Autophagy is a fundamental cellular process that maintains homeostasis and cell integrity, under stress conditions. Although the involvement of autophagy in various conditions has been elucidated, the role of autophagy in renal structure is not completely clarified. Our aim was to investigate the cytoprotective effect of autophagy against acute kidney injury (AKI) through cisplatin deteriorative pathway, which leads to AKI via renal cell degradation. For in vivo experiments, male Sprague Dawley rats were divided in to 2 groups (n = 6/group) as control, Cis-5D. Following a single intraperitoneal injection of cisplatin, rats were sacrificed after 5 days. Blood urea nitrogen (BUN), creatinine (Cr) and histological alterations were examined. Further, expression of key regulators of autophagy, light-clain 3 (LC3), p62, and Beclin1, was evaluated by immunohistochemistry (IHC). The rats exhibited severe renal dysfunction, indicated by elevated BUN, Cr. Hematoxylin and eosin staining revealed histological damages in cisplatin-treated rats. Furthermore, IHC analysis revealed increased expression of LC3, Beclin1 and decreased expression of p62. Furthermore, expression of aforementioned autophagy markers was restricted to proximal tubule. Taken together, our study demonstrated that cisplatin can cause nephrotoxicity and lead to AKI. This phenomenon accelerated autophagy in renal proximal tubules and guards against AKI.

      • KCI등재

        Effects of Albizia julibrissin Durazz through Suppression of Mitochondrial Fission and Apoptosis in Cisplatin-induced Acute Kidney Injury

        Hui-Ju Lee,김경현,김예지,Sung-Pil Cho,Geum-Lan Hong,정주영 한국생약학회 2022 Natural Product Sciences Vol.28 No.4

        Albizia julibrissin Durazz. (AJ; family Minosaceae) is widely distributed worldwide, and its stem bark has been used as a traditional herbal medicine. Acute kidney injury (AKI) is a clinical syndrome that results in sudden loss of renal function. This study aimed to investigate the effects of AJ against cisplatin-induced AKI using a human kidney proximal tubule epithelial cell line (HK-2) and cisplatin-treated mice. In vitro, cisplatin treatment increased apoptosis in HK-2 cells. However, AJ treatment decreased apoptosis of cisplatin-treated HK-2 cells. In vivo, cisplatin treatment accelerated renal injury by increasing the levels of renal injury markers, such as blood urea nitrogen, creatinine, kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin, which were reversed by AJ treatment. Histopathologically, AJ treatment resulted in decreased renal damage with less tubular necrosis and brush border desquamation compared with the AKI group. Additionally, cisplatin treatment upregulated mitochondrial fission, a pathological characteristic of AKI, which was downregulated by AJ treatment. Along with increased mitochondrial fission, AJ treatment also reduced cisplatin-induced apoptosis. These results suggest that AJ may be a potential therapeutic agent for cisplatin-induced AKI.

      • KCI등재

        Extract of Ranunculus sceleratus Reduced Adipogenesis by Inhibiting AMPK Pathway in 3T3-L1 Preadipocytes

        김예지(Yae-Ji Kim),조성필(Sung-Pil Cho),이희주(Hui-Ju Lee),홍금란(Geum-Lan Hong),김경현(Kyung-Hyun Kim),류시윤(Si-Yun Ryu),정주영(Ju-Young Jung) 한방비만학회 2022 한방비만학회지 Vol.22 No.1

        Objectives: Adipogenesis is the process by which pre-adipocytes are differentiated into adipocytes. It also plays an important role in adipocyte formation and lipid accumulation. Ranunculus sceleratus (R. sceleratus) extracts are used for the treatment of various diseases such as hepatitis, jaundice, and tuberous lymphadenitis in oriental medicine. However, its effect on adipogenesis has not yet been studied. In this study, we investigated the effects of R. sceleratus on adipogenesis in 3T3-L1 cells. Methods: Cells were treated with 50, 100, and 200 μg/ml of R. sceleratus and cell viability was evaluated. To differentiate the 3T3-L1 preadipocytes, a 3-isobutyl-1-methylxanthine, dexamethasone, and insulin (MDI) solution were used. The accumulation of lipid droplets was determined by Oil Red O staining. The expression levels of adipogenesis-related proteins were also determined. Results: MDI solution differentiated the preadipocytes into adipocytes and accumulation of lipids was observed in the differentiated 3T3-L1 cells. Interestingly, the amount of lipid droplets was reduced after R. sceleratus treatment. In addition, the expression levels of key adipogenic transcription factors, such as CCAAT/enhancer-binding proteins-α (C/EBP- α) and peroxisome proliferator-activated receptors-γ (PPAR-γ) were also reduced after R. sceleratus treatment. Furthermore, R. sceleratus increased AMP-activated kinase (AMPK) phosphorylation and decreased sterol regulatory element-binding protein-1 expression. Conclusions: Our results showed that R. sceleratus reduced preadipocyte differentiation by inhibiting C/EBP-α and PPAR-γ levels via the AMPK pathway. Therefore, we suggest that R. sceleratus may be potentially used as an anti-adipogenic agent.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼