Mitigating Effects of Tanacetum balsamita L. on Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD).
Rositsa MihaylovaReneta GevrenovaAlexandra PetrovaYonko SavovDimitrina Zheleva-DimitrovaVessela BalabanovaGeorgi Tsv MomekovRumyana SimeonovaPublished in: Plants (Basel, Switzerland) (2024)
The metabolic syndrome and its associated co-morbidities have been recognized as predisposing risk factors for the development of metabolic-associated fatty liver disease (MAFLD). The present study reports on the beneficial effect of the Tanacetum balsamita methanol-aqueous extract (ETB) at 150 and 300 mg/kg bw on biochemical parameters related to oxidative stress, metabolic syndrome, and liver function in rat animal models with induced MAFLD. ETB was found to be non-toxic with LD50 > 3000 mg/kg and did not affect cell viability of hepatic HEP-G2 cells in a concentration up to 800 μg/mL. The pathology was established by a high-calorie diet and streptozotocin. Acarbose and atorvastatin were used as positive controls. At the higher dose, ETB reduced significantly ( p < 0.05) the blood glucose levels by about 20%, decreased lipase activity by 52%, total cholesterol and triglycerides by 50% and 57%, respectively, and restored the amylase activity and leukocytes compared to the MAFLD group. ETB ameliorated oxidative stress biomarkers reduced glutathione and malondialdehyde in a dose-dependent manner. At 300 mg/kg, the beneficial effect of the extract on antioxidant enzymes was evidenced by the elevated catalase, glutathione peroxidase, and superoxide dismutase activity by 70%, 29%, and 44%, accordingly, compared to the MAFLD rats. ETB prevents the histopathological changes related to MAFLD. ETB, rich in 3,5-dicafeoylquinic, chlorogenic, and rosmarinic acids together with the isorhamnetin- and luteolin-glucoside provides a prominent amelioration of MAFLD.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- metabolic syndrome
- blood glucose
- dna damage
- ischemia reperfusion injury
- insulin resistance
- weight loss
- emergency department
- uric acid
- high fat diet
- adipose tissue
- cell proliferation
- cell cycle arrest
- type diabetes
- heat shock
- cardiovascular disease
- mouse model
- cell death
- endothelial cells