Background: Obesity is a complex multifactorial disease characterized by excessive adiposity, and is linked to an increased risk of nonalcoholic fatty liver disease (NAFLD). Flavonoids are natural polyphenolic compounds that exert interesting pharmacological effects as antioxidant, anti-inflammatory, and lipid-lowering agents. In the present study, we investigated the possible therapeutic effects of the flavonoid chrysin on obesity and NAFLD in rats, and the role of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathways in mediating these effects. Method: Thirty-two Wistar male rats were divided into two groups: the control group and the obese group. Obesity was induced by feeding with an obesogenic diet for 3 months. The obese rats were subdivided into four subgroups, comprising an untreated group, and three groups treated orally with different doses of chrysin (25, 50, and 75 mg/kg/day for one month). Results revealed that chrysin treatment markedly ameliorated the histological changes and significantly and dose-dependently reduced the weight gain, hyperglycemia, and insulin resistance in the obese rats. Chrysin, besides its antioxidant boosting effects (increased GSH and decreased malondialdehyde), activated the AMPK pathway and suppressed the mTOR and lipogenic pathways, and stimulated expression of the genes controlling mitochondrial biogenesis in the hepatic tissues in a dose-dependent manner. In conclusion, chrysin could be a promising candidate for the treatment of obesity and associated NAFLD, aiding in attenuating weight gain and ameliorating glucose and lipid homeostasis and adipokines, boosting the hepatic mitochondrial biogenesis, and modulating AMPK/mTOR/SREBP-1c signaling pathways.

Oxidative stress associated with long-term glucocorticoids administration is a route through which secondary osteoporosis can be developed. The therapeutic potential of Phoenix dactilyfera L. pits is offered by their balanced, valuable and diverse phytochemical composition providing protective potential against oxidative reactions, making it a good candidate to treat glucocorticoid-induced osteoporosis (GIO). This study evaluates the possible anti-osteoporotic effect of date pit extract (DPE) against dexamethasone (DEXA)-induced osteoporosis. Male rats were allocated into three control groups, which received saline, low and high doses of DPE (150 and 300 mg/kg/day), respectively. Osteoporosis-induced groups that received DEXA (1 mg/kg/day) were divided into DEXA only, DPE (2 doses) + DEXA, and ipriflavone + DEXA. Femoral bone minerals density and bone mineral content, bone oxidative stress markers, Wnt signaling, osteoblast and osteoclast differentiation markers, and femur histopathology were evaluated. DPE defeated the oxidative stress, resulting in ameliorative changes in Wnt signaling. DPE significantly reduced the adipogenicity and abolished the osteoclastogenic markers (RANKL/OPG ratio, ACP, TRAP) while enhancing the osteogenic differentiation markers (Runx2, Osx, COL1A1, OCN). In Conclusion DPE restored the balanced proliferation and differentiation of osteoclasts and osteoblasts precursors. DPE can be considered a promising remedy for GIO, especially at a low dose that had more potency.

Objective: To assess the role of miRNA712_3p as a specific biomarker in early detection of toxoplasmosis in plasma of mice acutely infected with Toxoplasma gondii. Methods: Real-time PCR was used to measure the level of miRNA712_3p in plasma of infected mice. Immune-competent and immune-suppressed mice were examined, three and five days post-infection. Results: Results revealed significant up-regulation of plasma miRNA712_3p in both immune- competent and immune-compromised groups in comparison to the control non-infected group. Additionally, an increase in the level of miRNA712_3p was noticed correspondently in the parasite density detected in liver impression smears. Conclusions: miRNA712_3p can be used as a novel biomarker for the detection of Toxoplasma gondii infection in both immune-competent and immune-compromised host.