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