FOLLOWUS
1. Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan,China
2. Department of Nephrology, Wuhan Integrated Traditional Chinese Medicine and Western Medicine Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan,China
纸质出版日期:2016,
网络出版日期:2014-12-9,
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Zhao, L., Jiang, Sj., Lu, Fe. et al. Effects of berberine and cinnamic acid on palmitic acid-induced intracellular triglyceride accumulation in NIT-1 pancreatic β cells., Chin. J. Integr. Med. 22, 496–502 (2016). https://doi.org/10.1007/s11655-014-1986-0
Li Zhao, Shu-jun Jiang, Fu-er Lu, et al. Effects of berberine and cinnamic acid on palmitic acid-induced intracellular triglyceride accumulation in NIT-1 pancreatic β cells[J]. Chinese Journal of Integrative Medicine, 2016,22(7):496-502.
Zhao, L., Jiang, Sj., Lu, Fe. et al. Effects of berberine and cinnamic acid on palmitic acid-induced intracellular triglyceride accumulation in NIT-1 pancreatic β cells., Chin. J. Integr. Med. 22, 496–502 (2016). https://doi.org/10.1007/s11655-014-1986-0 DOI:
Li Zhao, Shu-jun Jiang, Fu-er Lu, et al. Effects of berberine and cinnamic acid on palmitic acid-induced intracellular triglyceride accumulation in NIT-1 pancreatic β cells[J]. Chinese Journal of Integrative Medicine, 2016,22(7):496-502. DOI: 10.1007/s11655-014-1986-0.
To investigate the effects of berberine (BBR) and cinnamic acid (CA)
the main active components in Jiaotai Pill (交泰丸
JTP)
on palmitic acid (PA)-induced intracellular triglyceride (TG) accumulation in NIT-1 pancreatic β cells. Cells were incubated in culture medium containing PA (0.25 mmol/L) for 24 h. Then treatments with BBR (10 μmol/L)
CA (100 μmol/L) and the combination of BBR and CA (BBR+CA) were performed respectively. Intracellular lipid accumulation was assessed by Oil Red O staining and TG content was measured by colorimetric assay. The expression of adenosine monophosphate-activated protein kinase (AMPK) protein and its downstream lipogenic and fatty acid oxidation genes
including fatty acid synthase (FAS)
acetyl-coA carboxylase (ACC)
phosphorylation acetyl-coA carboxylase (pACC)
carnitine acyl transferase 1 (CPT-1) and sterol regulating element binding protein 1c (SREBP-1c) were determined by Western blot or real time polymerase chain reaction. PA induced an obvious lipid accumulation and a significant increase in intracellular TG content in NIT-1 cells. PA also induced a remarkable decrease in AMPK protein expression and its downstream targets such as pACC and CPT-1. Meanwhile
AMPK downstream lipogenic genes including SREBP-1c mRNA
FAS and ACC protein expressions were increased. Treatments with BBR and BBR+CA
superior to CA
significantly reversed the above genes changes in NIT-1 pancreatic β cells. However
the synergistic effect of BBR and CA on intracellular TG content was not observed in the present study. It can be concluded that in vitro
BBR and BBR+CA could inhibit PA-induced lipid accumulation by decreasing lipogenesis and increasing lipid oxidation in NIT-1 pancreatic β cells.
To investigate the effects of berberine (BBR) and cinnamic acid (CA)
the main active components in Jiaotai Pill (交泰丸
JTP)
on palmitic acid (PA)-induced intracellular triglyceride (TG) accumulation in NIT-1 pancreatic β cells. Cells were incubated in culture medium containing PA (0.25 mmol/L) for 24 h. Then treatments with BBR (10 μmol/L)
CA (100 μmol/L) and the combination of BBR and CA (BBR+CA) were performed respectively. Intracellular lipid accumulation was assessed by Oil Red O staining and TG content was measured by colorimetric assay. The expression of adenosine monophosphate-activated protein kinase (AMPK) protein and its downstream lipogenic and fatty acid oxidation genes
including fatty acid synthase (FAS)
acetyl-coA carboxylase (ACC)
phosphorylation acetyl-coA carboxylase (pACC)
carnitine acyl transferase 1 (CPT-1) and sterol regulating element binding protein 1c (SREBP-1c) were determined by Western blot or real time polymerase chain reaction. PA induced an obvious lipid accumulation and a significant increase in intracellular TG content in NIT-1 cells. PA also induced a remarkable decrease in AMPK protein expression and its downstream targets such as pACC and CPT-1. Meanwhile
AMPK downstream lipogenic genes including SREBP-1c mRNA
FAS and ACC protein expressions were increased. Treatments with BBR and BBR+CA
superior to CA
significantly reversed the above genes changes in NIT-1 pancreatic β cells. However
the synergistic effect of BBR and CA on intracellular TG content was not observed in the present study. It can be concluded that in vitro
BBR and BBR+CA could inhibit PA-induced lipid accumulation by decreasing lipogenesis and increasing lipid oxidation in NIT-1 pancreatic β cells.
Berberinecinnamic acidpalmitic acidNIT-1 cellslipidChinese MedicineJiaotai Pill
Berberinecinnamic acidpalmitic acidNIT-1 cellslipidChinese MedicineJiaotai Pill
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