Purslane ( <i>Portulaca oleracea</i> L.) Extract Attenuates Obesity-Induced Inflammation and Enhances Mitochondrial Biogenesis <i>via</i> the miR-221/222 and AMPK/SIRT1 Axis in Rats

Purslane (<i>Portulaca oleracea</i> L.) exhibits anti-inflammatory and antioxidant properties, but its role in regulating adipose tissue inflammatory microRNAs and mitochondrial biogenesis in skeletal muscle under high-fat diet (HFD) conditions remains unclear. This study aimed to evaluate the effects of purslane extract (PE) on HFD-induced inflammation and mitochondrial biogenesis, focusing on regulation of the miR-221/222 cluster in white adipose tissue (WAT) and the AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) axis in skeletal muscle. Male Sprague-Dawley rats were divided into four groups: normal chow diet, HFD, HFD+0.2% PE, and HFD+0.4% PE for 12 weeks. PE supplementation significantly reduced body weight gain, improved serum and hepatic lipid profiles, and decreased circulating inflammatory cytokines (<i>P</i><0.05). In WAT, PE reduced expression of pro-inflammatory cytokines and M1 macrophage markers while increasing expression of a M2 marker. Additionally, PE inhibited phospho-nuclear factor-kappa B levels and suppressed miR-221/222 expression in WAT. In skeletal muscle, PE enhanced the expression of genes related to mitochondrial biogenesis and restored mitochondrial content. Furthermore, PE increased AMPK, total SIRT, and SIRT1 activities, supporting its role in improving mitochondrial function in skeletal muscle. These findings suggest that the beneficial effects of PE against HFD-induced obesity are mediated, at least in part, by suppression of the WAT miR-221/222 cluster and activation of the AMPK/SIRT1 axis in skeletal muscle, thereby alleviating inflammation and enhancing mitochondrial biogenesis.