HPLC-PDA and in vivo anti-inflammatory potential of isorhamnetin-3-O-β-D-glucoside from Zygophyllum simplex L.

Ethnopharmacological Relevance: Inflammation is a biological process in response to injury, resulting in altered blood flow, increased vascular permeability, tissue destruction, and the production of reactive oxygen species (ROS) and inflammatory mediators. Zygophyllum simplex L., a medicinal plant traditionally used in the Arabian Peninsula for inflammatory disorders, has demonstrated promising in vitro anti-inflammatory activity due to its phenolic content.

Empagliflozin protects the heart from atrial fibrillation in rats through inhibiting the NF-κB/HIF-1α regulatory axis and atrial remodeling.

Atrial fibrillation (AF) is the most common form of sustained cardiac arrhythmia. The current study aimed to investigate the potential of empagliflozin (EMPA) to protect against acetylcholine (ACh)/calcium chloride (CaCl)-induced AF in rats and elucidate the possible underlying mechanism of action. Rats were randomly assigned to five groups, as follows: CTRL group: received 1 ml/kg isotonic saline; AF group: received 1 ml/kg induction mixture of ACh/CaCl (60 µg ACh and 10 mg CaCl per ml); EMPA group: received 30 mg/kg EMPA; AF + EMPA10 group: received the induction mixture concurrent with 10 mg/kg EMPA; AF + EMPA30 group: received the induction mixture concurrent with 30 mg/kg EMPA.

Targeting Nrf2/HO-1 and NF-κB/TNF-α signaling pathways with empagliflozin protects against atrial fibrillation-induced acute kidney injury in rats.

A bidirectional relationship exists between atrial fibrillation (AF) and kidney function. Uncontrolled AF may lead to kidney injury, whereas renal dysfunction may contribute to AF initiation and maintenance. This study aimed to investigate the protective effect of the sodium glucose cotransporter-2 inhibitor empagliflozin (EMPA) on acute kidney injury (AKI) associated with AF induced by acetylcholine and calcium chloride (ACh/CaCl) in rats and elucidate the potential underlying mechanism.