Objective   To explore improvement effect of plant sterol ester of α-linolenic acid (ALA-PS) on non-alcoholic fatty liver disease (NAFLD) and its underlying mechanism in mice.

  Methods  After one week′s adaptive feeding, 50 male C57BL/6J mice were randomly divided into five groups: a control group with normal diet, a model group with high fat diet (HFD), a plant sterol group (PS) with HFD added by 2% PS, an α-linolenic acid (ALA) group with HFD added by 1.3% ALA, and a plant sterol ester of α-linolenic acid group (ALA-PS) with HFD added by 3.3% ALA-PS, respectively. By the end of 16 weeks′ continuous treatment, the body weight and liver index of all the mice were determined; serum and liver tissue triglyceride (TG) and total cholesterol (TC) were measured. Hematoxylin-eosin (HE) staining was used to observe lipid accumulation and steatosis in liver tissues; endoplasmic reticulum morphology was examined with transmission electron microscopy. Protein expressions of c-Jun amino-terminal kinase (JNK), phospho-JNK (p-JNK), B cell lymphoma 2 (Bcl-2) and Bcl-2-as-sociated X protein (Bax) were measured with Western blot.

  Results   Compared with that in the control mice, a large amount of lipid accumulation was observed in the model mice. Improved hepatic steatosis and restored hepatic endoplasmic reticulum were examined and significantly decreased TG and TC in serum and liver tissues were detected in the mice of ALA-PS group (both P < 0.05). Significantly decreased protein expression of p-JNK and Bcl-2 and increased protein expression of Bcl-2 were also detected in the mice of ALA-PS group.

  Conclusion   ALA-PS could effectively improve NAFLD induced by high-fat diet and the underlying mechanism of the effect may related to the inhibition of apoptosis caused by endoplasmic reticulum stress.