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A convenient and efficient copper-catalyzed oxidative C3-cyanoarylation of quinoxalin-2(1H)-ones is developed using 3-aminoindazoles as efficient arylating agents via the cleavage of two C–N bonds.

Four ruthenium(II) polypyridyl complexes were synthesized and characterized by elemental analysis, IR, ESI-MS and 1H NMR. The in vitro cytotoxicities of the complexes against BEL-7402, HeLa, A549, HepG2 and MG-63 cancer cells were investigated by MTT methods, giving IC50 values ranging from 6.9 to 43.5 μM. The complexes show their highest inhibitory effect on MG-63 cells, but no cytotoxic activities against HeLa cells. Cellular uptake experiments indicate that the complexes can enter the cytoplasm and accumulate in the cell nuclei. The complexes can induce apoptosis in MG-63 cells, enhance the levels of reactive oxygen species, and induce a decrease in mitochondrial membrane potential. The cell cycle distribution shows that the complexes induce cell cycle arrest at S phase in MG-63 cells. Additionally, these complexes can up-regulate the levels of Bad and Bid expression and down-regulate the expression of Bcl-2 and Bcl-x.

In this article, the in vitro cytotoxicity of platycodin D was evaluated in human PC-12, SGC-7901, BEL-7402, HeLa and A549 cancer cell lines. PC-12 cells were sensitive to platycodin D treatment, with an IC50 value of 13.5±1.2μM. Morphological and comet assays showed that platycodin D effectively induced apoptosis in PC-12 cells. Platycodin D increased the levels of reactive oxygen species (ROS) and induced a decrease in mitochondrial membrane potential. Platycodin D induced cell cycle arrest at the G0/G1 phase in the PC-12 cell line. Platycodin D can induce autophagy. In addition, platycodin D can down-regulate the expression of Bcl-2 and Bcl-x, and up-regulate the levels of Bid protein in the PC-12 cells. The results demonstrated that platycodin D induced PC-12 cell apoptosis through a ROS-mediated mitochondrial dysfunction pathway.

Four new ruthenium(II) polypyridyl complexes [Ru(dmb)2(dqtbt)](ClO4)2 (1) (dqtbt=12-(2,3-diphenyl-quinoxalin-6-yl)-4,5,10,13-tetraazabenzo[b]triphenylene, dmb=4,4'-dimethyl-2,2'-bipyridine), [Ru(bpy)2(dqtbt)](ClO4)2 (2) (bpy=2,2'-bipyridine), [Ru(phen)2(dqtbt)](ClO4)2 (3) (phen=1,10-phenanthroline) and [Ru(dmp)2(dqtbt)](ClO4)2 (4) (dmp=2,9-dimethyl-1,10-phenanthroline) were synthesized and characterized. The cytotoxicity in vitro of the complexes was evaluated against human BEL-7402, A549, HeLa, HepG-2 and MG-63 cancer cell lines. These complexes are sensitive to BEL-7402 cells, the IC50 values are 4.9±0.5, 4.6±0.4, 7.7±1.8 and 1.9±0.3μM toward BEL-7402 cells. The complexes can increase the levels of reactive oxygen species and induce the decrease of mitochondrial membrane potential. Morphological and comet assay studies show that the complexes can effectively induce apoptosis in BEL-7402 cells. Complexes 1-4 inhibit the cell growth at G0/G1 phase in BEL-7402 cell line. The complexes can downregulate the expression of Bcl-2 and Bcl-x proteins and upregulate the levels of Bid protein in BEL-7402 cells. The results show that the complexes induce BEL-7402 cell apoptosis through a ROS-mediated mitochondrial dysfunction pathway. In addition, the complexes show strong protein-binding affinities.

A new ligand Adbdp and its four ruthenium(II) polypyridyl complexes [Ru(N-N)2(Adbdp)](ClO4)2 [N-N = dmb: 4,4′-dimethyl-2,2′-bipyridine 1, bpy: 2,2′-bipyridine 2, phen: 1,10-phenanthroline 3 and dmp: 2,9-dimethyl-1,10-phenanthroline 4, Adbdp = acenaphtheno[2,3-b]-1,4-diazabenzo[i]dipyrido[3,2-a:2′,3′-c]phenazine] were synthesized and characterized by elemental analysis, ESI-MS and 1H NMR. The cytotoxicity in vitro of the complexes against BEL-7402, HeLa, MG-63 and A549 cells was studied by MTT method. The IC50 values are 24.2 ± 1.9, 11.5 ± 3.6, 3.4 ± 0.3 and 9.7 ± 0.5 μM for complexes 1, 2, 3 and 4 toward A549 cells, respectively. The apoptosis was assayed with AO/EB and Hoechst 33258 staining methods. The cellular uptake was investigated with DAPI-stained cell nuclei. The reactive oxygen species and mitochondrial membrane potential were performed under fluorescent microscope. The cell cycle distribution was studied by flow cytometry and the protein expression of Bcl-2 family proteins was analyzed by western blot. The results show that the complexes induce A549 cell apoptosis through a ROS-mediated mitochondrial dysfunction pathway.

Two positional isomers of dibenzoxanthenes C1 and C2 were synthesized and characterized. The crystal structures of the compounds were solved by single-crystal X-ray diffraction. Binding the two compounds with CT-DNA (calf thymus DNA)/BSA (bovine serum albumin) was thoroughly investigated by UV-Vis and fluorescence spectroscopy. The compounds interact with DNA through an intercalative mode and show strong affinities with BSA. Their cytotoxicity upon irradiation was investigated in vitro using the MTT method. By comparing the two isomers, C1 and C2, compound C2 showed greater enhanced therapeutic potential upon irradiation with visible light. Significant nuclear damage of HeLa cells was observed after a comet assay. These compounds inhibited cell growth in HeLa cells at the S phase. These compounds have been found to induce apoptosis in HeLa cells using AO/EB staining experiments and flow cytometry. The two compounds can enhance the intracellular reactive oxygen species and decrease the mitochondrial membrane potential. The compounds activated caspase-3, caspase-7, procaspase-7 and down-regulated the expression levels of the anti-apoptotic proteins Bcl-2 and Bcl-x, and up-regulated the expression levels of the pro-apoptotic proteins Bax and Bim. The compounds induced apoptosis of HeLa cells via a ROS-mediated mitochondrial dysfunction pathway.

A Ru(II) polypyridyl complex [Ru(bpy)2(HMSPIP)](ClO4)2 (1) (bpy=2,2'-bipyridine, HMSPIP=2-(4-methylsulfonyl)phenyl-1H-imidazo[4,5-f][1,10] phenanthroline) was synthesized. The IC50 value of the complex against human hepatocellular cell BEL-7402 is 21.6±2.7 μM. The complex shows no cytotoxic activity toward human lung adenocarcinoma cell A549, human osteosarcoma cell MG-63 and human breast cancer cell SK-BR-3 cells. It is easily for complex 1 to be taken up by BEL-7402 cells. The complex can enhance the reactive oxygen species (ROS) levels and induce the decrease in the mitochondrial membrane potential. The complex inhibits the cell growth in BEL-7402 cells at G2/M phase. Complex 1 can regulate the expression of Bcl-2 family proteins. The results show that the complex induces apoptosis of BEL-7402 cells through a ROS-mediated mitochondrial dysfunction pathway.

In the present study, the in vitro cytotoxicity of daidzein was evaluated in human BEL-7402, A549, HeLa, HepG-2 and MG-63 cancer cell lines. BEL-7402 cells were sensitive to daidzein treatment, with an IC50 value of 59.7±8.1 µM. Daidzein showed no cytotoxic activity toward A549, HeLa, HepG-2 and MG-63 cells. Daidzein increased the levels of reactive oxygen species (ROS) and induced a decrease in mitochondrial membrane potential. Morphological and comet assays showed that daidzein effectively induced apoptosis in BEL-7402 cells. Additionally, daidzein caused cell cycle arrest at the G2/M phase in the BEL-7402 cell line. Daidzein downregulated the expression of Bcl-2, Bcl-x and Baid proteins and upregulated the levels of Bim protein in the BEL-7402 cells. The results demonstrated that daidzein induced BEL-7402 cell apoptosis through an ROS-mediated mitochondrial dysfunction pathway.

Two new ruthenium(II) polypyridyl complexes [Ru(dmb)2(dcdppz)](ClO4)2 (1) and [Ru(bpy)2(dcdppz)](ClO4)2 (2) were prepared and characterized. The crystal structure of the complex 2 was solved by single crystal X-ray diffraction. The complex crystallizes in the monoclinic system, space group P21/n with a=12.9622(14)Å, b=17.1619(19)Å, c=22.7210(3)Å, β=100.930(2)(°), R=0.0536, Rω=0.1111. The DNA-binding constants for complexes 1 and 2 were determined to be 1.92×10(5) (s=1.72) and 2.24×10(5) (s=1.86)M(-1), respectively. The DNA-binding behaviors showed that complexes 1 and 2 interact with DNA by intercalative mode. The antioxidant activities of the ligand and the complexes were performed. Ligand, dcdppz, has no cytotoxicity against the selected cell lines. Complex 1 shows higher cytotoxicity than complex 2, but lower than cisplatin toward selected cell lines. The apoptosis and cell cycle arrest were investigated, and the apoptotic mechanism of BEL-7402 cells was studied by reactive oxygen species (ROS), mitochondrial membrane potential and western blot analysis. Complex 1 induces apoptosis in BEL-7402 cells through ROS-mediated mitochondrial dysfunction pathway and by regulating the expression of Bcl-2 family proteins.

Four new ruthenium(II) polypyridyl complexes [Ru(dmb)2(DHBT)](ClO4)2 (1) (DHBT = 12,14-dihydroxyl-4,5,9,10,11,13-hexaazabenzo[b]triphenylene, dmb = 4,4′-dimethyl-2,2′-bipyridine), [Ru(bpy)2(DHBT)](ClO4)2 (2) (bpy = 2,2′-bipyridine), [Ru(phen)2(DHBT)](ClO4)2 (3) (phen = 1,10-phenanthroline) and [Ru(dmp)2(DHBT)](ClO4)2 (4) (dmp = 2,9-dimethyl-1,10-phenanthroline) were synthesized and characterized. The cytotoxicity in vitro of these complexes was evaluated against human HepG-2, HeLa, A549, MG-63 and BEL-7402 cancer cell lines. The IC50 values of the complexes toward selected cell lines range from 14.9 ± 1.1 to 30.1 ± 2.7 μM. The cytotoxicity and the levels of reactive oxygen species were found to increase with increasing concentrations of the complexes. The complexes are sensitive to MG-63 cells and can inhibit the MG-63 cell migration. Morphological and comet assay studies show that the complexes can effectively induce apoptosis in MG-63 cells. Complex 2 inhibits the cell growth at the G0/G1 phase, whereas the other complexes exhibit the antiproliferative mechanism at the S phase in the MG-63 cell line. The complexes can downregulate the expression of Bcl-2 protein and upregulate the levels of Bad protein in MG-63 cells. The complexes induce MG-63 cells apoptosis through a ROS-mediated mitochondrial dysfunction pathway.

Two Ru(II) polypyridyl complexes [Ru(dmb)2(idpq)](ClO4)2 (1) (idpq = indeno[1,2-b]dipyrido[3,2-f:2′,3′-h]-quinoxaline-6-one, dmb = 4,4′-dimethyl-2,2′-bipyridine) and [Ru(bpy)2(idpq)](ClO4)2 (2) (bpy = 2,2′-bipyridine) have been synthesized and characterized. Their in vitro cytotoxicities, apoptosis, cellular uptake, production of reactive oxygen species (ROS), mitochondrial membrane potential assays and effects on cell cycle distribution were studied. The IC50 values range from 13.1 ± 1.1 to 30.9 ± 3.1 μM. Complex 1 is toxic to HeLa cells with an IC50 value of 13.1 ± 1.1 μM, while complex 2 shows relatively high cytotoxicity against HepG-2 cells. However, both complexes exhibit lower cytotoxicity than cisplatin toward selected cell lines under identical conditions. Both complexes can induce apoptosis and cell cycle arrest at the S and G0/G1 phases in HeLa cells, respectively. In addition, both Ru(II) complexes, which can be effectively taken up by HeLa cells, induced generation of intracellular ROS in a concentration-dependent manner and produced a decrease in mitochondrial membrane potential. The results show that these complexes induce apoptosis in HeLa cells through a ROS-mediated mitochondrial dysfunction pathway.

A new ligand dmdppz and its four ruthenium(II) polypyridyl complexes [Ru(dmb) 2 (dmdppz)](ClO 4 ) 2 ( 1 ), [Ru(bpy) 2 (dmdppz)](ClO 4 ) 2 ( 2 ), [Ru(phen) 2 (dmdppz)](ClO 4 ) 2 ( 3 ) and [Ru(dmp) 2 (dmdppz)](ClO 4 ) 2 ( 4 ) (where dmb, bpy, phen, dmp and dmdppz stand for 4,4′-dimethyl-2,2′-bipyridine, 2,2′-bipyridine, 1,10-phenanthroline, 2,9-dimethyl-1,10-phenanthroline and 5,8-dimethoxylpyrido[3,2- a :2′,3′- c ]phenazine, respectively) have been synthesized and characterized. Their DNA binding behaviors show that the complexes bind to calf thymus DNA by intercalation. The complexes exhibit efficient photocleavage of pBR322 DNA on irradiation. The cytotoxicity of the ligand and the complexes toward HepG-2, HeLa, MG-63, A549 and BEL-7402 were assayed by MTT ((3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyltetrazolium bromide)) method. The IC 50 values of the complexes 1 , 2 , 3 and 4 toward BEL-7402 cells are 14.6, 16.8, 18.0 and 16.7 μM, respectively. Dmdppz shows no cytotoxic activity against selected cell lines. The cellular uptake, apoptosis, comet assay, reactive oxygen species (ROS), mitochondrial membrane potential and western blot analysis were investigated. These results indicate that complexes 1 – 4 exert their toxicity through the intrinsic ROS-mediated mitochondrial pathway, which is accompanied by the regulation of Bcl-2 family proteins.

Two Ru(II) polypyridyl complexes [Ru(phen) 2 (idpq)](ClO 4 ) 2 ( 1 ) and [Ru(dmp) 2 (idpq)](ClO 4 ) 2 ( 2 ) were synthesized and characterized. Cytotoxicity, apoptosis, cell cycle arrest, reactive oxygen species and mitochondrial membrane potential were assayed. The IC 50 values of complexes 1 and 2 toward HepG-2, A549, MG-63 and HeLa cell lines range from 15.1 ± 2.1 to 24.8 ± 2.4 μM. The complexes can effectively induce apoptosis and induce cell cycle arrest at G0/G1 phase by an increase of 4.88% for 1 and 6.64% for 2 at G0/G1 phase in HeLa cells. Complexes 1 and 2 can enter the cytoplasm and accumulate in the nuclei. The complexes can enhance the level of reactive oxygen species. The ratio of the red/green is 0.74 and 0.52 for complexes 1 and 2 , which suggests that the complexes induce a decrease of mitochondrial membrane potential. These complexes induce apoptosis in HeLa through ROS-mediated mitochondrial dysfunction pathway.

Three Ru(II) polypyridyl complexes [Ru(dmb)2(HMSPIP)](ClO4)2 (1), [Ru(phen)2(HMSPIP)](ClO4)2 (2) and [Ru(dmp)2(HMSPIP)](ClO4)2 (3) were synthesized and characterized. The cytotoxicity in vitro, apoptosis, cell cycle arrest, reactive oxygen species and mitochondrial membrane potential were assayed. The IC50 values of complexes 1, 2 and 3 toward BEL-7402, A549, MG-63 and SK-BR-3 cell lines ranged from 10.9 ± 1.6 to 42.0 ± 3.4 μM. Complexes 1, 2 and 3 can effectively induce apoptosis and inhibit the growth of BEL-7402 cells at the G2/M phase. These complexes can enhance the level of reactive oxygen species and induce decrease in the mitochondrial membrane potential. Additionally, complex 2 can down-regulate the expression of antiapoptotic protein of Bcl-2 protein and up-regulate the levels of proapoptotic protein Bim in BEL-7402 cells.

A new Ru(II) polypyridyl complex [Ru(phen)2(addppn)](ClO4)2 (Ru1) has been synthesized and characterized. The DNA-binding constant of the complex with DNA was determined to be 1.93 (±0.12) × 106 M−1. The complex interacts with DNA by an intercalative mode. Cytotoxicity in vitro, apoptosis, cell cycle distribution, apoptotic pathway, reactive oxygen species and mitochondrial membrane potential assays were performed. The IC50 values of Ru1 toward BEL-7402, HeLa, MG-63 and SKBR-3 cell lines are 3.9 ± 0.4, 9.0 ± 0.8, 6.6 ± 0.6 and 5.1 ± 0.6 μM, respectively. Interestingly, Ru1 shows a higher cytotoxicity than cisplatin on BEL-7402 cells under identical conditions. Ru1 can effectively induce apoptosis in BEL-7402 and induces cell cycle arrest at the G0/G1 phase in BEL-7402 cells and at the G2/M phase in SKBR-3 cells. In addition, Ru1 can enhance the level of reactive oxygen species and induce the decrease of the mitochondrial membrane potential. Western blot analysis shows that Ru1 activates caspase-3 and -7, down-regulates the expression of the anti-apoptotic proteins of Bcl-x and Bag-1, and upregulates the levels of the proapoptotic proteins of Bad, Bak, Bax and Bim in BEL-7402 cells. These results show that Ru1 induces apoptosis in BEL-7402 cells through an ROS-mediated mitochondrial dysfunction pathway.

In this paper, the problem of designing a adaptive threshold for Fault diagnostic in Full Authority Digital Engine Control system that are subject to environmental disturbances and various input is investigated. According to aero-engine small deviation linearization model, state matrix perturbation model with "soft boundary" pseudo normal distribution is built. The proposed algorithm bases on satisfaction filtering principle. Linear matrix inequality (LMI) method is applied to get upper bound of residual. With the residual distribution probability model and the target false alarm rate, the optimal threshold is determined. The proposed algorithm is then applied to sensor fault detection on a turbofan aero-engine. Simulation results demonstrate and validate the performance and capability of the adaptive threshold algorithm.

Four new ruthenium(II) polypyridyl complexes [Ru(N-N)2(dhbn)](ClO4)2 (N-N = dmb: 4,4'-dimethyl-2,2'-bipyridine 1; bpy = 2,2'-bipyridine 2; phen = 1,10-phenanthroline 3; dmp = 2,9-dimethyl-1,10-phenanthroline 4) were synthesized and characterized. The cytotoxicity in vitro of the ligand and complexes toward HepG-2, HeLa, MG-63 and A549 were assayed by MTT method. The IC50 values of the complexes against the above cells range from 17.7 ± 1.1 to 45.1 ± 2.8 μM. The cytotoxic activity of the complexes against HepG-2 cells follows the order of 4 > 2 > 3 > 1. Ligand shows no cytotoxic activity against the selected cell lines. Cellular uptake, apoptosis, comet assay, reactive oxygen species, mitochondrial membrane potential, cell cycle arrest, and the expression of proteins involved in apoptosis pathway induced by the complexes were investigated. The results indicate that complexes 1-4 induce apoptosis in HepG-2 cells through an intrinsic ROS-mediated mitochondrial dysfunction pathway.

The DNA-binding, photocleavage, and antitumor activity of three free base pyridyl corroles 1, 2, and 3 have been investigated. The binding affinity toward CT-DNA decreases with increasing number of pentafluorophenyl, whereas the photocleavage activity toward pBR322 DNA becomes more efficient. Singlet oxygen was demonstrated as active species responsible for DNA cleavage. These corroles exhibited high cytotoxicity against three tested cancer cells (Hela, HapG2, and A549) and the cytotoxicity could be further enhanced under irradiation. Intracellular reactive oxygen species level was also monitored using HeLa Cells upon the combined treatment of corroles and light. These corroles could be absorbed by HeLa cells at low concentration. They can induce the decrease of mitochondrial membrane potential and apoptosis of tumor cells under irradiation.

Four new ruthenium(II) polypyridyl complexes [Ru(dmb)2(DQTT)](ClO4)2 (1) (DQTT = 12-(1,4-dihydroquinoxalin-6-yl)-4,5,9,14-tetraazabenzo[b]triphenylene, dmb = 4,4′-dimethyl-2,2′-bipyridine), [Ru(bpy)2(DQTT)](ClO4)2 (2) (bpy = 2,2′-bipyridine), [Ru(phen)2(DQTT)](ClO4)2 (3) (phen = 1,10-phenanthroline) and [Ru(dmp)2(DQTT)](ClO4)2 (4) (dmp = 2,9-dimethyl-1,10-phenanthroline) were synthesized and characterized by elemental analysis, ESI-MS, 1H NMR and 13C NMR. The cytotoxic activity in vitro of the complexes was evaluated against human BEL-7402, A549, HeLa, HepG-2 and MG-63 cancer cell lines by MTT (3-(4,5-dimethylthiazole)-2,5-diphenyltetrazolium bromide) method. The IC50 values of complexes 1–4 against BEL-7402 cells are 31.8 ± 1.0, 35.8 ± 1.6, 29.0 ± 0.8 and 25.0 ± 0.9 μM, respectively. The morphological apoptosis was investigated with AO/EB (acridine orange/ethidium bromide) and Hoechst 33258 staining methods. The DNA damage was assayed by comet assay. The inhibition of cell migration was evaluated by the wound healing assay. The levels of ROS (reactive oxygen species) and the changes of mitochondrial membrane potential were studied under fluorescent microscope. The percentages in the cells of apoptotic and necrotic cells and the cell cycle arrest were determined by flow cytometry. The expression of Bcl-2 family proteins was investigated by western blot analysis. The results show that the complexes induce BEL-7402 cells apoptosis through a ROS-mediated mitochondrial dysfunction pathway, which was accompanied by regulation of the expression of Bcl-2 family proteins.

Two dibenzoxanthene isomers 3 and 4 were synthesized and characterized. The crystal structures of the two compounds were solved by single-crystal X-ray diffraction. Binding of two compounds with calf thymus DNA (CT DNA) and BSA (bovine serum albumin) has been thoroughly investigated by UV-Vis and fluorescence spectroscopy. The DNA-binding constants were determined to be 2.51 (± 0.09) × 10(3) for compound 3 and 4.55 (± 0.10) × 10(3) for compound 4. Two compounds can cleave pBR322 DNA upon irradiation. Significant nuclear damages of BEL-7402 cells were observed with compound treatment in a comet assay. The cytotoxicity in vitro was investigated by MTT method. These compounds have been found to induce nuclear condensation and fragmentation in BEL-7402 cells. The two compounds can enhance intracellular reactive oxygen species and decrease the mitochondrial membrane potential. The compounds activated caspase-3 and caspase-7, down-regulated the expression levels of anti-apoptotic protein Bcl-2, and up-regulated the expression levels of pro-apoptotic protein Bax. These compounds induce apoptosis of BEL-7402 cells through an ROS-mediated mitochondrial dysfunction pathway.

A new ruthenium(II) polypyridyl complex [Ru(dmp)2(pddppn)](ClO4)2Ru1 was synthesized and characterized. The cytotoxic activity in vitro of the complex was evaluated by MTT method. Ru1 shows high effect on the inhibition of the cell growth against BEL-7402, HeLa, MG-63 and A549 cells with low IC50 values of 1.6±0.4, 9.0±0.8, 1.5±0.2 and 1.5±0.3 μM, respectively. The cellular uptake indicates that Ru1 can enter into the cytoplasm and accumulate in the cell nuclei. Ru1 can induce apoptosis in A549 cells and enhance the levels of reactive oxygen species (ROS) and induce the decrease of mitochondrial membrane potential. In addition, Ru1 can down-regulate the levels of Bcl-2, Bcl-x, Bak, and Bim expression and up-regulate the expression of Bag-1 and Bad. The complex induces apoptosis of A549 cells through an intrinsic ROS-mediated mitochondrial dysfunction pathway, which was accompanied by regulating the expression of caspases and Bcl-2 family proteins.

The aim of our study was to investigate DNA-binding and cytotoxic activity of the four new Ru(II) polypyridyl complexes [Ru(dmb)₂(HMHPIP)](ClO₄)₂ (1), [Ru(bpy)₂(HMHPIP)](ClO₄)₂ (2), [Ru(phen)₂(HMHPIP)](ClO₄)₂ (3) and [Ru(dmp)₂(HMHPIP)](ClO₄)₂ (4). The complexes interact with DNA through intercalative mode and show relatively high cytotoxic activity against A549 cells, no cytotoxicity toward MG-63 cells. Complexes 1-4 can enhance the levels of ROS in A549 cells and induce the decrease of the mitochondrial membrane potential. These complexes inhibit the cell growth in A549 cells at G0/G1 or S phase. Complex 3 activated caspase 7, and down-regulated the expression of the anti-apoptotic protein Bcl-2. Complexes 1-4 induce apoptosis in A549 cells through ROS-mediated mitochondrial dysfunction pathway.