PMID- 30338826
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20211204
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 19
DP  - 2018 Oct
TI  - Protective effect of cyclosporine on inflammatory injury of renal tubular 
      epithelial cells.
PG  - 6551-6559
LID - 16071 [pii]
LID - 10.26355/eurrev_201810_16071 [doi]
AB  - OBJECTIVE: This study aims to explore the protective effect of cyclosporine on 
      inflammation-induced renal tubular epithelial cells and its potential mechanism. 
      MATERIALS AND METHODS: Human kidney-2 (HK-2) cells were induced by transforming 
      growth factor-beta (TGF-beta) for constructing an inflammatory injury model. Cells were 
      then treated with different concentrations of cyclosporine for further 
      investigating the biological functions. Cell viability was detected via cell 
      counting kit-8 assay (CCK-8). The cytotoxicity was detected via lactate 
      dehydrogenase (LDH) release assay. Expression levels of cell damage factors and 
      mammalian target of rapamycin (mTOR) pathway-related genes were detected via 
      polymerase chain reaction (PCR), immunofluorescence and Western blotting, 
      respectively. RESULTS: TGF-beta inhibited the viability of HK-2 cells, increased 
      expressions of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and 
      apoptosis-related genes. Cyclosporine treatment greatly reversed the cell damage 
      on HK-2 cells induced by TGF-beta. Expression levels of mTOR pathway-related genes 
      were downregulated after cyclosporine treatment. CONCLUSIONS: Cyclosporine 
      protects HK-2 cells from inflammatory injury via regulating mTOR pathway.
FAU - Zhang, Y-Q
AU  - Zhang YQ
AD  - Department of Nephrology, The Affiliated Jiangyin Hospital of Southeast 
      University Medical College, Wuxi, China. 13626238242@163.com.
FAU - Chen, Y
AU  - Chen Y
FAU - Ding, Y-M
AU  - Ding YM
FAU - Yu, T-H
AU  - Yu TH
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (IL1B protein, human)
RN  - 0 (Interleukin-1beta)
RN  - 0 (TNF protein, human)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Cell Line
MH  - Cyclosporine/*pharmacology
MH  - Cytoprotection
MH  - Epithelial Cells/*drug effects/metabolism/pathology
MH  - Humans
MH  - Interleukin-1beta/metabolism
MH  - Kidney Tubules/*drug effects/metabolism/pathology
MH  - Nephritis, Interstitial/metabolism/pathology/*prevention & control
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Transforming Growth Factor beta/toxicity
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2018/10/20 06:00
MHDA- 2019/12/18 06:00
CRDT- 2018/10/20 06:00
PHST- 2018/10/20 06:00 [entrez]
PHST- 2018/10/20 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
AID - 16071 [pii]
AID - 10.26355/eurrev_201810_16071 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Oct;22(19):6551-6559. doi: 
      10.26355/eurrev_201810_16071.