Etoricoxib treatment prevented body weight gain and ameliorated oxidative stress in the liver of high-fat diet-fed rats.
Fariha KabirKamrun NaharMd Mizanur RahmanFariha MamunShoumen LaskerFerdous KhanTahmina YasminKhondker Ayesha AkterNusrat SubhanMd Ashraful AlamPublished in: Naunyn-Schmiedeberg's archives of pharmacology (2020)
The main focus of this study was to determine the role of etoricoxib in counterbalancing the oxidative stress, metabolic disturbances, and inflammation in high-fat (HF) diet-induced obese rats. To conduct this study, 28 male Wistar rats (weighing 190-210 g) were distributed randomly into four groups: control, control + etoricoxib, HF, and HF + etoricoxib. After 8 weeks of treatment with etoricoxib (200 mg/kg), all the animals were sacrificed followed by the collection of blood and tissue samples in order to perform biochemical tests along with histological staining on hepatic tissues. According to this study, etoricoxib treatment prevented the body weight gain in HF diet-fed rats. Furthermore, rats of HF + etoricoxib group exhibited better blood glucose tolerance than the rats of HF diet-fed group. In addition, etoricoxib also markedly normalized HF diet-mediated rise of hepatic enzyme activity. Etoricoxib treatment lowered the level of oxidative stress indicators significantly with a parallel augmentation of antioxidant enzyme activities. Furthermore, etoricoxib administration helped in preventing inflammatory cell invasion, collagen accumulation, and fibrotic catastrophe in HF diet-fed rats. The findings of the present work are suggestive of the helpful role of etoricoxib in deterring the metabolic syndrome as well as other deleterious pathological changes afflicting the HF diet-fed rats.
Keyphrases
- oxidative stress
- weight gain
- weight loss
- high fat diet
- acute heart failure
- physical activity
- body mass index
- adipose tissue
- insulin resistance
- ischemia reperfusion injury
- heart failure
- type diabetes
- bariatric surgery
- diabetic rats
- skeletal muscle
- cardiovascular disease
- replacement therapy
- systemic sclerosis
- endoplasmic reticulum stress
- cardiovascular risk factors