# Ethanol extract of Garcinia kola seeds alleviates HGHFD/STZ-induced nonalcoholic fatty liver disease in diabetic rats by modulating oxidative stress, inflammation, and lipid accumulation

## TL;DR

This study shows that an extract from Garcinia kola seeds can reduce liver damage in diabetic rats by lowering oxidative stress, inflammation, and fat buildup.

## Contribution

The novel finding is that Garcinia kola extract reduces nonalcoholic fatty liver disease in diabetic rats by modulating the SREBP-1c pathway.

## Key findings

- EGK reduced blood glucose levels and improved liver lipid accumulation in diabetic rats.
- EGK inhibited oxidative stress and inflammation in both rat models and HepG2 cells.
- EGK downregulated the SREBP-1c pathway, which is linked to lipid metabolism.

## Abstract

To investigate the ameliorative effects of Garcinia kola ethanol extract (EGK) on type 2 diabetes mellitus (T2DM) combined with nonalcoholic fatty liver disease (NAFLD) and to explore its underlying mechanisms.

In vivo, a T2DM rat model was established using HGHFD/STZ. In vitro, HepG2 cells were induced with FFA to create a model of lipid accumulation. Lipid accumulation (LA), oxidative stress (OS) levels, and inflammatory markers were measured using kit methods. Additionally, the expression of the SREBP-1c pathway was detected by immunohistochemistry and western blot (WB) to further understand the potential mechanism of EGK’s protective effect on diabetic liver injury.

In vivo, EGK significantly reduced blood glucose levels (P<0.01), restored body weight (P<0.01), and improved liver LA, OS, and inflammatory levels (P<0.01) in diabetic rats. Histopathological results indicated that EGK effectively ameliorated diabetes-induced liver injury. Immunohistochemistry and WB results revealed that EGK significantly down-regulated the expression of the SREBP-1c pathway (P<0.01). In vitro, EGK markedly improved lipid accumulation, oxidative stress, and inflammation levels in HepG2 cells (P<0.01). Immunofluorescence and WB results showed that EGK significantly reduced the expression of the SREBP-1c pathway (P<0.01).

EGK alleviates T2DM combined with NAFLD by reducing lipid accumulation through the inhibition of oxidative stress, inflammatory responses, and the SREBP-1c signaling pathway.