Yuyan Han

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease across the world. Once it progresses to non-alcoholic steatohepatitis (NASH), little can be done to reverse the damage. A potential treatment for NASH is cannabigerol (CBG), as it has shown anti-inflammatory effects in other models, although, little is known about its effects on NASH. Mast cells (MCs) play a role in mediating the progression of NASH. Their concentration in the liver directly correlates to levels of fibrosis. Therefore, we aim to evaluate levels of MC infiltration under CBG treatment in a NASH-induced mouse model. C57BL/6 mice were fed with a methionine/choline-deficient (MCD) or control (CTR) diet for 3 weeks, then divided into 3 sub-groups. The mice were injected with vehicle, low CBG [2.46 mg/kg/day], or high CBG [24.6 mg/kg/day] for another two weeks. The livers were harvested and frozen to be sliced for placement on slides. Slides were stained for presence of MCs using Toluidine-blue (T-blue) stain and Naphthol A-SD chloroacetate-esterase (CAE) stain. The samples were observed under a microscope and evaluated for mast cell infiltration. Co-staining of FcɛR1 (a MC biomarker) and TGFβ1 (a pro-inflammatory cytokine) was used to stain the co-localization of MCs and their inflammatory effect using immunofluorescence. We have found that treatment with low CBG decreased the numbers of MCs in MCD mice while high CBG treatment did not. There was no positive staining of MCs in the control groups. These results are consistent with the FcɛR1/TGFβ1 immunofluorescence staining. There was no positive staining for mast cells in the control groups and treatment with low CBG decreased the presence of mast cells and TGFβ1 expression. In conclusion, low CBG treatment reduced MC infiltration caused by the MCD diet in the mice. High CBG treatment did not reduce MC infiltration in the mice.

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