The effects and mechanisms of berberine on proliferation of papillary thyroid cancer K1 cells induced by high glucose
10.3760/cma.j.issn.0578-1426.2017.07.007
- VernacularTitle:小檗碱对高糖诱导的甲状腺乳头状癌K1细胞增殖的影响及机制
- Author:
Jing NI
;
Fang WANG
;
Ling YUE
;
Guangda XIANG
;
Linshuang ZHAO
;
Yong WANG
;
Lizi YE
;
Jing DONG
- Keywords:
Berberine;
Papillary thyroid cancer;
High glucose
- From:
Chinese Journal of Internal Medicine
2017;56(7):507-511
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect and mechanisms of berberine (BBR) on the proliferation of papillary thyroid cancer K1 cells induced by high glucose.Methods K1 cells were cultured under 5.5 mmol/L or 25 mmol/L glucose condition with or without different concentration of BBR (0,10,40 and 80 μmol/L) for 24 hours.The proliferations of K1 cells in each condition were detected by MTT.Western blot was used to measure the expression of nuclear factor erythroid 2-related factor 2 (Nrt2),phosphoinositide 3-kinase (PI3K),protein kinase B (Akt) and phosphorylated-Akt (p-Akt).The distribution pattern of Nrf2 in K1 cells was determined using immunofluorescent staining.Results Compared with 5.5 mmol/L condition,the proliferation rate [(126.64 ± 5.41) % vs (87.31 ± 3.67) %],expression levels of PI3K (0.425 ±0.019 vs 0.272 ±0.039),p-Akt/Akt (0.446 ±0.021 vs 0.168 ±0.035) and Nrf2 (0.597 ± 0.014 vs 0.308 ± 0.026),and Nrf2 distribution (93.0% vs 23.1%) in nuclear of K 1 cells under 25 mmol/L condition were significantly elevated,respectively (all P <0.01).Addition of BBR in 25 mmol/L condition dose dependently (10,40,80 μmol/L) lowered the proliferation rate of K1 cells [(111.76 ± 4.10)%,(70.03 ±2.18)%,(32.41 ±3.76)% vs (126.64 ±5.41)%,all P<0.05],and suppressed the expression of PI3K,p-Akt/Akt,Nrf2,and Nrf2 nuclear distribution (P < 0.05).Conclusions BBR dose dependently inhibited the proliferation of high glucose-induced K1 cells.This effect was associated with the suppression on of PI3K/Akt signaling activation,Nrf2 expression and its nuclear translocation.