Objective To establish qualityrep resentation and correlation analysis method of Ligustrum lucidum Ait.(Glossy Privet Fruit,Nüzhenzi)based on characteristic spectrum of drug system,so as to evaluate thequality of Nüzhenzi decoction pieces accurately and comprehensively.Methods Usinges-tablished HPLC-PDA method to represent the quality of Nüzhenzi characteristic spectrum of drug system. Then the qualitative representation of 14 batches of Nüzhenzi decoction pieces was based on the quantity and type of characteristic peaks of specific chromatograms,the quantitative representation of 14 batches of Nüzhenzi pieces was based on the content of four characteristic index components including salidroside, tyrosol,specnuezhenide and quercetin and the sum of iridoids (using specnuezhenide for representation)and flavonoids (using quercetin for representation ), then correlation analysis was based on the representation results of quantity and quality respectively in 14 batches of Nüzhenzi pieces referenced to thebenchmarkdecoctionpiece.Results TakingLot.S10as the benchmark,in Nüzhenzi HPLCspecific chromatogram there were 1 1 characteristic peaks which were common in all batches,including two benzene glycosides peaks ,five iridoids peaks,four flavonoids peaks.The contents of effective index components in batch S14,S12,S5,S8,S9,S6 and S11 were higher,with the highest correlation in S14, S12,S5,S8,S9 and S10,so the quality of S5,S8,S9,S12,and S14 were superior to other batches. Conclusion The evaluation model of qualityrep resentation and correlation analysis of Nüzhenzispecific chromatogram concerning on correlation of the overall quality and the effectiveness of the application,can effectively and accurately evaluate the quality of Nüzhenzi.

AIM: To investigate the role of sorafenib in promoting ferroptosis in HCC, and whether cell death can be induced by activating mitochondrial oxidative stress and consequent mitochondrial dysfunction. METHODS: Hepatocellular carcinoma cell lines Huh7 and HCC-LM3 were treated with different concentrations of sorafenib, the cell viability was determined by CCK-8 assay; mitochondrial membrane potential (MMP) was measured by Tetramethylrhodamine (TMRM) staining; The mitochondrial oxygen consumption rate was monitored by the Seahorse XF24 Analyzer; mitochondrial superoxide indicator (Mitosox) was used to determine the level of reactive oxygen species (ROS) in mitochondria; the formation of total ROS was determined by dichlorofluorescein diacetate (DCF-DA) staning. Finally, The recovery of oxidative damage and cell death induced by sorafenib was observed after pretreated by glutathione (GSH). RESULTS: With the increasing concentration of sorafenib, the survival of the Huh7 and HCC-LM3 was significantly decreased. Sorafenib also inhibited the oxygen consumption rate and decreased oxidative phosphorylation, which results in the depolarization of MMP, ROS accumulation and eventually ferroptosis of HCC cells. However, the occurrence of oxidative stress induced by sorafenib in HCC cells can be effectively reversed by the pretreatment of GSH. CONCLUSION: The ferroptosis can be induced by sorafenib through inducing mitochondrial dysfunction and ROS accumulation in HCC cells. However, the GSH can restore oxidative damage. Therefore, induction of the GSH deficiency in HCC may be a potential therapeutic option to enhance the efficacy of sorafenib.