rat proximal tubular epithelial nrk52e cells  (ATCC)

Journal: Molecular Medicine Reports

Article Title: β-elemene attenuates IRI-AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF-κB/MAPK signal axis activation

doi: 10.3892/mmr.2025.13586

Figure Lengend Snippet: β-elemene protects NRK52E cells from H 2 O 2 -induced inflammation. (A) Optimal duration of H 2 O 2 treatment in NRK52E cells was identified by employing the CCK-8 assay. (B) CCK-8 analysis was employed to identify the ELE impact on viability of NRK52E cells. (C) NRK52E cells underwent pretreatment with various doses of ELE and were treated for 6 h with or without 600 µM H 2 O 2 . CCK-8 analysis was used to determine cell viability. Reverse transcription-quantitative PCR was employed to evaluate the mRNA expression of (D) IL-1β, (E) TNF-α, (F) MCP-1 and (G) ICAM-1. *P<0.05, **P<0.01, ***P<0.001. CCK-8, Cell Counting Kit-8; OD, optical density; ELE, β-elemene; ns, not significant; MCP-1, monocyte chemoattractant protein-1; ICAM-1, intercellular adhesion molecule 1.

Article Snippet: Rat proximal tubular epithelial NRK52E cells were obtained from American Type Culture Collection.

Techniques: CCK-8 Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Cell Counting

Journal: Molecular Medicine Reports

Article Title: β-elemene attenuates IRI-AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF-κB/MAPK signal axis activation

doi: 10.3892/mmr.2025.13586

Figure Lengend Snippet: ELE inhibits the inflammatory response by suppressing TLR4/MyD88/NF-κB pathway activation in vivo and in vitro . (A) Renal p-P65, MyD88, TLR4 and P65 expression. (B) Western blotting of the p-P65, MyD88, TLR4 and P65 expression in NRK52E cells treated with H 2 O 2 and various concentrations of ELE. *P<0.05, **P<0.01. ELE, β-elemene; IRI, ischemia-reperfusion injury; TLR4, toll-like receptor 4; MyD88, myeloid differentiation primary response gene 88; p-, phosphorylated-; ns, not significant.

Article Snippet: Rat proximal tubular epithelial NRK52E cells were obtained from American Type Culture Collection.

Techniques: Activation Assay, In Vivo, In Vitro, Expressing, Western Blot

Journal: Molecular Medicine Reports

Article Title: β-elemene attenuates IRI-AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF-κB/MAPK signal axis activation

doi: 10.3892/mmr.2025.13586

Figure Lengend Snippet: ELE ameliorates H 2 O 2 -induced NRK52E cell apoptosis. (A) TUNEL assay; scale bar, 50 µm. (B) Bax, c-caspase3, Bcl-2 and caspase-3 protein expression were measured using western blotting. (C) CCK-8 analysis was performed to identify the NAC impact on viability of NRK52E cells. (D) Identification and semi-quantification of Bax, c-caspase3, Bcl-2 and caspase-3 protein expression in NRK52E cells. *P<0.05, **P<0.01. ELE, β-elemene; c-, cleaved; ns, not significant; OD, optical density; NAC, N-Acetylcysteine.

Article Snippet: Rat proximal tubular epithelial NRK52E cells were obtained from American Type Culture Collection.

Techniques: TUNEL Assay, Expressing, Western Blot, CCK-8 Assay

Journal: Molecular Medicine Reports

Article Title: β-elemene attenuates IRI-AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF-κB/MAPK signal axis activation

doi: 10.3892/mmr.2025.13586

Figure Lengend Snippet: ELE decreases inflammatory and apoptosis signaling by inhibiting MAPK signaling pathway activation. (A) ERK, p-JNK, p-P38, JNK, p-ERK and P38 in the kidney. (B) Identification and semi-quantification of p-JNK, p-ERK1/2, p-P38, JNK, ERK1/2 and P38 expression in NRK52E cells. *P<0.05, **P<0.01. ELE, β-elemene; IRI, ischemia-reperfusion injury; ns, not significant; p-, phosphorylated.

Article Snippet: Rat proximal tubular epithelial NRK52E cells were obtained from American Type Culture Collection.

Techniques: Activation Assay, Expressing

Journal: Molecular Medicine Reports

Article Title: β-elemene attenuates IRI-AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF-κB/MAPK signal axis activation

doi: 10.3892/mmr.2025.13586

Figure Lengend Snippet: MyD88 knockdown suppresses apoptosis and MAPK signaling pathway activation in H 2 O 2 -treated NRK52E cells. (A) MyD88 expression in NRK52E cells. (B) MyD88, Bax, c-caspase3, Bcl-2, JNK, caspase-3 p-ERK, p-JNK, ERK, p-P38 and P38 expression in NRK52E cells treated with H 2 O 2 . *P<0.05, **P<0.01. c-, cleaved; p-, phosphorylated; ns, not significant; si, small interfering.

Article Snippet: Rat proximal tubular epithelial NRK52E cells were obtained from American Type Culture Collection.

Techniques: Knockdown, Activation Assay, Expressing

Journal: Scientific Reports

Article Title: Renal Damaging Effect Elicited by Bicalutamide Therapy Uncovered Multiple Action Mechanisms As Evidenced by the Cell Model

doi: 10.1038/s41598-019-39533-3

Figure Lengend Snippet: MTT assay of NRK52E- and RMC cells affected by testosterone, bicalutamide, and R1881 in 25 mM hyperglycemic medium. NRK52E cell line (1 × 10 4 cells/well) on 24-well plate was incubated in medium containing 5% bovine serum and 0.4% PBS overnight until adhered. Finally, the medium was replaced fresh with serum free medium. RMC cell line (1 × 10 4 cells/well) on 24-well plate was incubated in medium containing 25 mM glucose, 15% FBS, 0.4% PBS, and 0.8% G418 overnight until adhered. Finally, the medium was replaced fresh with 2% FBS. At final step, the two cells were simultaneously treated as indicated. ( a ) NRK52E + testosterone (1~10 3 nM), ( b ) NRK52E + bicalutamide (3.75~60 μM), ( c ) RMC + testosterone (1~10 3 nM), ( d ) RMC + R1881 (1~10 3 nM), and ( e ) RMC + bicalutamide, and ( f ) RMC + bicalutamide + testosterone for duration as indicated. Experiment was performed in triplicate

Article Snippet: NRK52E, a rat normal renal proximal tubular epithelial cell line; and RMC, the rat mesangial cell line, were provided by the Bioresource Collection & Research Center (BCRC; Hsinchu, Taiwan).

Techniques: MTT Assay, Incubation