A series of thiophene derivatives (TPs) were synthesized and evaluated for cytotoxicity in HepG2 and SMMC-7721 cell lines by MTT assay. TP 5 was identified as a potential anticancer agent based on its ability to inhibit tumor cell growth. Drawbacks of TPs, including poor solubility and high toxicity, were overcome through delivery using self-assembling HSA nanoparticles (NPs). The optimum conditions for TP 5-NPs synthesis obtained by adjusting the temperature and concentration of TP 5. The NPs had an encapsulation efficiency of 99.59% and drug-loading capacity of 3.70%. TP 5 was slowly released from TP 5-NPs in vitro over 120 h. HepG2 and SMMC-7721 cell lines were employed to study cytotoxicity of TP 5-NPs, which exhibited high potency. ROS levels were elevated and mitochondrial membrane potentials reversed when the two cell lines were treated with TP 5-NPs for 12 h. Cellular uptake of fluorescence-labeled TP 5-NPs in vitro was analyzed by flow cytometry and laser confocal scanning microscopy. Fluorescence intensity increased over time, suggesting that TP 5-NPs were efficiently taken up by tumor cells. In conclusion, TP 5-NPs showed great promise as an anticancer therapeutic agent.

This study aimed to evaluate the analgesic efficacy of astilbin and its underlying mechanisms. Astilbin suppressed the symptoms of acetic acid–induced writhing, lengthened the latency period on the hot plate, and reduced the licking and biting response of formalin-injected mice, suggesting its analgesic efficacy on the central nervous system. Astilbin suppressed neuronal nitric oxide synthase and enhanced serotonin and norepinephrine in serum and brains of mice after 30 s of thermal stimulation, but it failed to influence their levels before thermal stimulation. Among six chosen antagonists, only nimodipine, a calcium channel blocker, strongly enhanced the abirritation of astilbin, as indicated by the lengthened latency period of mice treated with nimodipine plus astilbin in the hot plate test. The expression levels of c-Fos and phosphorylated calmodulin-dependent protein kinase II and c-Jun N-terminal kinase in the brains were reduced in the astilbin-treated mice. Astilbin-mediated analgesia is partially related to Ca²⁺ channels.