Copyright
©The Author(s) 2019.
World J Gastroenterol. May 28, 2019; 25(20): 2450-2462
Published online May 28, 2019. doi: 10.3748/wjg.v25.i20.2450
Published online May 28, 2019. doi: 10.3748/wjg.v25.i20.2450
Figure 3 Trimethylamine N-oxide alleviates liver injury by mitigating hepatic endoplasmic reticulum stress and cell death in rats fed a high-fat high-cholesterol diet.
A: Representative immunoblots from three rats in each group; B-E: Densitometric quantification from three rats in each group. Relative protein levels normalized to β-actin except for phosphorylated c-Jun N-terminal kinase (JNK), which was normalized to endogenous JNK. The data are presented as the mean ± SE (n = 3). aP < 0.05, vs rats fed a chow diet; bP < 0.01, vs rats fed a chow diet; cP < 0.05, vs rats fed a high-fat high-cholesterol diet; dP < 0.01, vs rats fed a high-fat high-cholesterol diet. JNK: c-Jun N-terminal kinase; TMAO: Trimethylamine N-oxide; HFHC: High-fat high-cholesterol.
- Citation: Zhao ZH, Xin FZ, Zhou D, Xue YQ, Liu XL, Yang RX, Pan Q, Fan JG. Trimethylamine N-oxide attenuates high-fat high-cholesterol diet-induced steatohepatitis by reducing hepatic cholesterol overload in rats. World J Gastroenterol 2019; 25(20): 2450-2462
- URL: https://www.wjgnet.com/1007-9327/full/v25/i20/2450.htm
- DOI: https://dx.doi.org/10.3748/wjg.v25.i20.2450