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Baicalein (BAI) is a major constituent of Scutellaria baicalensis Georgi. Previous studies showed that BAI had obvious effects on U14 cervical tumor-bearing mice model and HeLa cells. However, the use of BAI is inconvenient and troublesome, due to its low oral bioavailability. The aim of this study was to develop baicalein-loaded nanoliposomes (BAI-LP) to improve its bioavailability. In this study, BAI-LP was prepared by thin film hydration method. The average size, polydispersity index (PDI), zeta potential and encapsulation efficiency (EE) of the BAI-LP were 194.6±2.08 nm, 0.17±0.025, −30.73±0.41 mV, and 44.3±2.98%, respectively. Drug storage stability study showed no significant changes in these values after 4 weeks of storing at 4 ∘ C. Additionally, Sulforhodamine B (SRB) experimental results indicated that the BAI-LP could achieve better anti-tumor effects than free BAI. The results of the experiment demonstrated that BAI-LP had a better antitumor effect with a higher inhibition rate of 66.34 ± 15.33% than free BAI with a inhibition rate of 41.89 ± 10.50% by using U14 cervical tumor-bearing mice model. In conclusion, the study suggested that BAI-LP would serve as a potent delivery vehicle for BAI in future cancer therapy.

Purpose: Remote ischemic preconditioning (RIPC) confers cardioprotection against ischemia reperfusion (IR) injury. However, the precise mechanisms involved in RIPC-induced cardioprotection are not fully explored. The present study was aimed to identify the role of melatonin in RIPC-induced late cardioprotective effects in rats and to explore the role of H 2 S, TNF-α and mitoK ATP in melatonin-mediated effects in RIPC. Methods: Wistar rats were subjected to RIPC in which hind limb was subjected to four alternate cycles of ischemia and reperfusion of 5 min duration by using a neonatal blood pressure cuff. After 24 h of RIPC or ramelteon-induced pharmacological preconditioning, hearts were isolated and subjected to IR injury on the Langendorff apparatus. Results: RIPC and ramelteon preconditioning protected the hearts from IR injury and it was assessed by a decrease in LDH-1, cTnT and increase in left ventricular developed pressure (LVDP). RIPC increased the melatonin levels (in plasma), H 2 S (in heart) and decreased TNF-α levels. The effects of RIPC were abolished in the presence of melatonin receptor blocker (luzindole), ganglionic blocker (hexamethonium) and mitochondrial K ATP blocker (5-hydroxydecanoic acid). Conclusions: RIPC produce delayed cardioprotection against IR injury through the activation of neuronal pathway, which may increase the plasma melatonin levels to activate the cardioprotective signaling pathway involving the opening of mitochondrial K ATP channels, decrease in TNF-α production and increase in H 2 S levels. Ramelteon-induced pharmacological preconditioning may also activate the cardioprotective signaling pathway involving the opening of mitochondrial K ATP channels, decrease in TNF-α production and increase in H 2 S levels.