Conclusions
TGJ may be a therapy for the NAFLD with T2DM rats by modulating the inflammatory response and the oxidative stress capacity.
Methods
NAFLD was induced in T2DM rat model. Male Wistar rats were assigned into six groups: Group I (control), Group II (model), Group III (pioglitazone, 0.5 mg/kg), Group IV (high dose of TGJ, 24.8 g/kg), Group V (middle dose of TGJ, 12.4 g/kg) and Group VI (low dose of TGJ, 6.2 g/kg). All rats in each group were treated with the corresponding drugs by gavage for 8 weeks. Haematoxylin and eosin analysis was conducted. The indicators of inflammatory and oxidative stress were analysed utilizing one-way ANOVA.
Objective
This study details the mechanism of TGJ on the treatment of NAFLD with T2DM. Materials and
Results
The contents of TNF-α (15.794 ± 3.302 pg/mL), IL-6 (76.801 ± 8.491 pg/mL), IL-1β (100.101 ± 13.150 pg/mL), CRP (1.052 ± 0.079 pg/mL) and MDA (3.972 ± 0.159 pg/mL) were obviously elevated in NAFLD with T2DM rats compared to controls. Except for the IL-6, the levels of other markers declined in a dose-dependent manner after treatment with TGJ. The SOD (14.139 ± 1.479 U/mgprot) and GSH-PX (81.511 ± 5.276 U/mgprot) levels significantly decreased in NAFLD with T2DM rats, while the levels of these indicators increased after treatment with TGJ. Conclusions: TGJ may be a therapy for the NAFLD with T2DM rats by modulating the inflammatory response and the oxidative stress capacity.