[The Effect of p-JAK1/p-STAT3 Signaling Way in Intervening NAFLD by Blueberry Probiotic Serum].

To explore the mechanism of interlukin-22 (IL-22)-mediated phosphor-Janus kinase-1(p-JAK1)/phosphor-signal transducer and activator of transcription 3 (p-STAT3) signaling way in the experiment of improving non-alcholic fatty liver disease (NAFLD) by blueberry probiotic serum.The rat serums with low-, medium-, and high-dose of 10% blueberry probiotics, as well as saline were prepared. NAFLD model was built by inducing normal liver cell line L-02 with free fatty acid (FFA).NAFLD model cells were cultured with saline serum (model group), low-, medium-, and high-dose blueberry probiotics serums (low-, medium-, and high-dose serum groups) , respectively .Normal liver cell group (normal group) was cultured with saline serum . Oil Red O staining was used to detect the lipid deposition in the cells; the intracellular level of triglyceride (TG) was quantitatively determined; the gene and protein expressions of IL-22, p-JAK1, p-STAT3, sterol-regulatory element binding protein-1c (SREBP-1c ) were detected by RT-PCR, Western blot and immunofluorescence methods.Twenty-four hours after modeling, a large amount of lipid deposition could be observed in model group. Compared with normal group, model group showed lower gene and protein expression levels of IL-22, p-JAK1 and p-STAT3 (P <0.01), and higher SREBP-1c and TG levels (P <0.01).Compared with model group, TG level and the lipid deposition in low-, medium-, and high-dose blueberry probiotics serum groups were gradually reduced. High-dose serum group showed higher gene and protein expression levels of IL-22, p-JAK1, p-STAT3 and lower SREBP-1c compared with the model, low-, and medium-dose serum groups (P <0.01). No significant [CM(155.3mm]differences in gene and protein levels between low- andmedium-doseserum groups were found (P >0.05).The blueberry probiotics could antagonize the NAFLD via p-JAK1/p-STAT3 signaling way.