Rats ; Animals ; Myocardial Reperfusion Injury/metabolism* ; Luteolin/metabolism* ; Down-Regulation ; Rats, Sprague-Dawley ; MicroRNAs/metabolism* ; Reperfusion Injury ; Apoptosis

Oral squamous cell carcinoma (OSCC) is a prevalent malignant tumor affecting the head and neck region (Leemans et al., 2018). It is often diagnosed at a later stage, leading to a poor prognosis (Muzaffar et al., 2021; Li et al., 2023). Despite advances in OSCC treatment, the overall 5-year survival rate of OSCC patients remains alarmingly low, falling below 50% (Jehn et al., 2019; Johnson et al., 2020). According to statistics, only 50% of patients with oral cancer can be treated with surgery. Once discovered, it is more frequently at an advanced stage. In addition, owing to the aggressively invasive and metastatic characteristics of OSCC, most patients die within one year of diagnosis. Hence, the pursuit of novel therapeutic drugs and treatments to improve the response of oral cancer to medication, along with a deeper understanding of their effects, remains crucial objectives in oral cancer research (Johnson et al., 2020; Bhat et al., 2021; Chen et al., 2023; Ruffin et al., 2023).
Humans ; Mouth Neoplasms/pathology* ; Carcinoma, Squamous Cell/metabolism* ; Luteolin/therapeutic use* ; Squamous Cell Carcinoma of Head and Neck/drug therapy* ; Head and Neck Neoplasms/drug therapy* ; Cell Line, Tumor

The study is aimed to explore the effects of stress at different temperatures( 35,45,55 ℃) on membrane permeability,active oxygen metabolism and accumulation of effective substances in Lonicera japonica,and provide theoretical basis for reducing deterioration and revealing browning mechanism during postharvest processing of L. japonica. The cell membrane permeability( relative conductivity,MDA content),active oxygen metabolism( SOD,POD,PPO,CAT activity) and the accumulation of effective substances( chlorogenic acid,luteolin,neochlorogenic acid,cryptochlorogenic acid,3,5-dicaffeoylquinic acid,3,4-dicaffeoylquinic acid and 4,5-dicaffeoylquinic acid) of L. japonica were all studied by constant temperature drying method,and the results were analyzed by the SPSS 17. 0 statistical software. The results showed that MDA content in L. japonica was increased by 151. 14% at 35 ℃,SOD,POD,PPO and CAT activity were 29. 73%,42. 86%,105. 02% and 10. 74% higher than at 45 ℃,respectively. The order of effective substance content in L. japonica was 35 ℃ >45 ℃ >55 ℃. The changes of membrane permeability,activity of active oxygen metabolizing enzyme and accumulation of active components were significantly affected by different temperature stress. The indexes showed that physiological and active oxygen metabolizing enzyme activity of L. japonica was the highest under 35 ℃ stress,chlorogenic acid and luteolin were effectively accumulated,which provides basic data for solving browning problem in the postharvest processing of L. japonica.
Cell Membrane Permeability ; Chlorogenic Acid/metabolism* ; Hot Temperature ; Lonicera/physiology* ; Luteolin/metabolism* ; Oxygen/metabolism* ; Stress, Physiological

OBJECTIVE: To study the effects of myo-inositol and luteolin on human lung cancer A549 cells and explore the possible mechanisms. METHODS: A549 cells were treated with different concentrations of myo-inositol and luteolin, either alone or in combination, and the cell viability was examined using MTT assay. A549 cells and human bronchial epithelial Beas-2B cells were treated for 48 h with 10 mmol/L myo-inositol and 20 μmol/L luteolin, alone or in combination, and the cell proliferation was detected using MTT assay; the colony formation and migration of the cells were examined with colony formation assay and wound healing assay, respectively. The protein expression levels in A549 cells were detected using Western blotting. RESULTS: Both myo-inositol and luteolin could dose-dependently inhibit the viability of A549 cells. Treatments with 10 mmol/L myo-inositol, 20 μmol/L luteolin, and both for 48 h caused significant reduction in the cell viability (92%, 83% and 70% of the control level, respectively) and colony number (79%, 73% and 43%, respectively), and significantly lowered the wound closure rate (24.61%, 13.08% and 8.65%, respectively, as compared with 29.99% in the control group). Similar treatments with myoinositol and luteolin alone or in combination produced no significant inhibitory effect on the growth, colony formation or migration of Beas-2B cells. The expressions of p-PDK1 and p-Akt in myo-inositol-treated A549 cells and the expression of pPDK1 in luteolin-treated cells were significantly decreased ( < 0.05), and the decrements were more obvious in the combined treatment group ( < 0.05). CONCLUSIONS Luteolin combined with myo-inositol can selectively inhibit the proliferation and migration of A549 cells, and these effects are probably mediated, at least in part, by suppressing the activation of PDK1 and Akt.
A549 Cells ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Humans ; Inositol ; administration & dosage ; therapeutic use ; Lung Neoplasms ; drug therapy ; metabolism ; Luteolin ; administration & dosage ; therapeutic use ; Protein-Serine-Threonine Kinases ; drug effects ; metabolism ; Proto-Oncogene Proteins c-akt ; drug effects ; metabolism ; Vitamin B Complex

OBJECTIVETo study the regulation of luteolin on spleen cells and sarcoma S180 cells in normal ICR mice.

METHODSSpleen cells and S180 cells were incubated with different concentrations of luteolin (50, 100, 200, and 400 μmol/L). The effect of luteolin on spleen cells and sarcoma S180 cells was determined by MTT assay. The apoptosis was detected using propidium iodide staining flow cytometry. Intracellular reactive oxygen species (ROS) was determined by flow cytometric analysis. Activities of free radicals scavenging were determined by hydroxyl radical and DPPH tests.

RESULTSCompared with the solvent control group, 200 and 400 μmol/L luteolin increased the spleen cells viability (P < 0.05). Luteolin at 100, 200, and 400 μmol/L decreased activities of S180 cells (P < 0.01). The proportion of sub-G1 phase spleen cells was reduced after treated with 200 and 400 μmol/L luteolin (P < 0.05). The proportion of sub-G1 phase S180 cells was elevated after treated with 200 and 400 μmol/L luteolin (P < 0.05). Compared with the solvent control group, levels of intracellular ROS in spleen cells of ICR mice all increased; levels of intracellular ROS in S180 cells all decreased after treated with 50, 100, 200, and 400 μmol/L luteolin (P < 0.05). Luteolin scavenged hydroxyl radical and DPPH in a dose dependent manner.

CONCLUSIONLuteolin had bilateral regulation on viability and apoptosis of spleen cells and S180 cells (promoting the viability of spleen cells, inhibiting apoptosis of spleen cells, inhibiting the viability of S180 cells, and promoting apoptosis of S180 cells), which was worth further study and exploration.

Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Cell Survival ; Luteolin ; metabolism ; Mice ; Mice, Inbred ICR ; Reactive Oxygen Species ; Sarcoma ; Spleen ; metabolism

This study analysed the tissue specific expression of critical genes involved in chlorogenic acid and luteolin biosynthesis, for exploiting the molecular mechanism of components biosynthesis in Lonicera confusa. Expression of PAL, 4CL, C4H, CHS, CHI, FNS and HQT gene families of chlorogenic acid and luteolin biosynthesis-related genes in buds and leaves of L. confusa were analyed by Real-time PCR. Expressions of PAL1, C4H1, 4CL1, CHS1, CHI3 and HQT2 in buds were lower than that in leaves, and expressions of PAL3, 4CL2, CHI2 and FNS2 in buds were higher than that in leaves. The results indicated that that PAL3 and 4CL2 may be associated with accumulation of chlorogenic acid, and the expression patterns of PAL1, CHS1, CHI3 and HQT2 in buds and leaves of L. confusa were different with L. japonica. This study provided some theoretical basis for the further research on genetic mechanism of active components differences in L. confusa and L. japonica.
Biosynthetic Pathways ; Chlorogenic Acid ; metabolism ; Gene Expression Regulation, Plant ; Lonicera ; genetics ; metabolism ; Luteolin ; biosynthesis ; Multigene Family ; Plant Proteins ; genetics ; metabolism

OBJECTIVETo observe the effect and mechanism of isoorientin from Gypsophila elegans on alcohol-induced hepatic fibrosis in rats.

METHODninety healthy male Wistar rats were randomly divided into six groups: the normal control group, the model control group, the colchicines group (positive control, 1.0 mg x kg(-1) x d(-1)), the high, middle and low-dose isoorientin groups (20, 50, 100 mg x kg(-1) x d(-1)). The normal control group received normal saline, while other groups received alcohol to cause hepatic fibrosis. After 24-weeks treatment, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), Interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), hyaluronic acid (HA), laminin (LN), type III precollagen (PCIII), hydroxyproline (Hyp), Myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were assayed according to the manufacturer's instructions, the alpha-SMA and TGF-beta1 were detected by western blotting, and the histopathological changes was observed by H&E staining.

RESULTIsoorientin could improve the liver function by decreasing the activity of ALT, AST, IL-6, TNF-alpha, MDA, MPO, HA, LN, PCIII and Hyp (P < 0.05), increasing the activity of SOD and GSH-Px (P < 0.05), and reducing the expression of alpha-SMA and TGF-beta1 (P < 0.05). In addition, the high and middle-dose isoorientin groups showed more remarkable effect

CONCLUSIONIsoorientin from G. elegans can protect hepatic fibrosis induced by alcohol.

Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Drugs, Chinese Herbal ; administration & dosage ; Ethanol ; adverse effects ; Glutathione Peroxidase ; blood ; Humans ; Liver Cirrhosis ; chemically induced ; drug therapy ; enzymology ; prevention & control ; Luteolin ; administration & dosage ; Male ; Protective Agents ; administration & dosage ; Rats ; Rats, Wistar ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVETo investigate the effect of luteolin on cell growth and apoptosis of HepG2 cells in vitro.

METHODSCultured HepG2,HL60,A549 and LO2 cells were treated with luteolin for different doses (0 μg/ml,2.5 μg/ml,10 μg/ml and 20 μg/ml) and varied times (0 h,24 h,48 h and 72 h). Cell viability was measured with MTT assay and IC50 was calculated. The reactive oxygen species (ROS) levels in HepG2 cells treated with luteolin for 6 h and 12 h were measured with flow cytometry. Cell apoptosis of HepG2 cells treated with luteolin for 24h was examined with flow cytometry and Annexin V-FITC/PI. Expression levels of apoptosis pathway proteins (p53,ASPP2 and iASPP) in HepG2 cells were detected with western blot and the dose and time-effect was analyzed.

RESULTSLuteolin effectively inhibited tumor cell proliferation in a dose-and time-dependent manner,and the inhibition rates of 20 μg/ml Luteolin for 72 h were 39.34%,62.90%,57.57% and 62.90% to LO2,HepG2, HL60 and A549 cells,respectively. The intracellular ROS level was decreased in HepG2 cells by 13.88% and 41.11% after being treated with luteolin for 6 h and 12 h,respectively. The apoptosis rate of HepG2 cells treated with luteolin for 24 h was 14.43%,and western blot showed that luteolin reduced the expression level of iASPP by 77.07% and up-regulated the expression of p53 by 179.37% and ASPP2 by 725.02% in HepG2 cells treated with luteolin for 12 h.

CONCLUSIONLuteolin has ant-proliferative and pro-apoptotic activity on hepatoma HepG2 cells, which is associated with the altered expression of pro-apoptotic factors and decreased ROS level in HepG2 cells.

Apoptosis ; drug effects ; Hep G2 Cells ; Humans ; Luteolin ; administration & dosage ; pharmacology ; Reactive Oxygen Species ; metabolism

The purpose of the present study was to investigate the effect of luteolin on the angiogenesis and invasion of breast cancer cells. MTT assay was used to examine breast cancer proliferation. The chick chorioallantoic membrane model was used to assess the angiogenesis effect. Wound healing assay was used to assess cell invasion ability. Western blot was used to analyze Bcl-2, AEG-1 and MMP-2 expression levels. The results showed luteolin inhibited MCF-7 cells proliferation in a dose- and time-dependent manner, and the expression of Bcl-2 protein was decreased. Luteolin had a strong anti-angiogenesis of chick chorioallantoic membrane. After treatment of MCF-7 cells with luteolin at 60 μmol/L for 48 h, migration rate was reduced by 71.07% compared with control (P < 0.01). After treatment of MCF-7 cells with luteolin at 60 μmol/L for 48 h, the expression of AEG-1 and MMP-2 was reduced by 82.34% (P < 0.05) and 85.70% (P < 0.05) respectively, compared with control. In conclusion, the results suggest that luteolin can inhibit the proliferation of breast cancer cells, and suppress the expression of Bcl-2. Furthermore, luteolin has strong anti-angiogenesis of chick chorioallantoic membrane and anti-invasive activity on breast cancer cells, and down-regulates the expression of AEG-1 and MMP-2.
Animals ; Breast Neoplasms ; pathology ; Cell Adhesion Molecules ; metabolism ; Cell Proliferation ; Chickens ; Chorioallantoic Membrane ; drug effects ; Down-Regulation ; Female ; Humans ; Luteolin ; pharmacology ; MCF-7 Cells ; Matrix Metalloproteinase 2 ; metabolism ; Neovascularization, Pathologic ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism

OBJECTIVETo study luteolin-induced non-small cell lung cancer cell line A549 apoptosis and the molecular mechanism for inhibiting its cycle arrest (G2 stage).

METHODMTT assay showed that luteolin had obvious inhibitory effect on A549 and indicated the half inhibition ratio (IC50). Cell cycle and apoptosis were detected by Hoechst 33258 nuclear staining assay, Annexin V-FITC/PI double staining and flow cytometry. Western blotting assay revealed changes in cycle and apoptosis-related proteins induced by luteolin. Possible molecular mechanism was suggested by Western blotting and immunocytochemistry.

RESULTLuteolin had an obvious growth inhibitory effect on A549 cells, with IC50 of 45.2 micromol x L(-1) at 48 h. Flow cytometry showed A549 cells mainly arrested in G2 stage after being treated by luteolin, with low expressions in cyclin A, p-CDC2 and p-Rb. Hoechst 33258 nuclear staining and Annexin V-FITC/PI double staining showed that the luteolin treatment group showed a significant apoptosis rate than the non-treatment group. Western blotting found luteolin can increase phosphorylation of JNK and decrease that of NF-kappaKB (p65). Immunocytochemistry results revealed luteolin can inhibit TNF-alpha-stimulated p65 from nuclear translocation as a transcription factor and thus promoting cell apoptosis.

CONCLUSIONLuteolin can obviously induce apoptosis of human non-small cell lung cancer cell A549 possibly by increasing phosphorylation of JNK to activate mitochondria apoptosis pathway, while inhibiting NF-kappaB from nuclear translocation as a transcription factor.

Annexin A5 ; metabolism ; Apoptosis ; drug effects ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Humans ; Luteolin ; pharmacology ; NF-kappa B ; metabolism