| | Type | Effect |
| | Butein | (i) Exhibited aldose reductase and advanced glycation end-products inhibition [57].
(ii) Protected pancreatic beta cells (INS-1 cells) against cytokine-induced toxicity mediated by inhibition of NO formation at concentrations of 15–30 μM [58].
(iii) Protected the murine hippocampal HT22 cells against glutamate-induced neurotoxicity, attenuated ROS generations through preserving the activities of SOD, GR, and GSH-Px [32].
(iv) Inhibited clonogenic growth of human breast cancer cells cocultured with fibroblasts.
(v) Inhibited prostate tumor growth in vitro and in vivo [59].
(vi) Inhibited NF-κB activation and reduces infiltration of inflammatory cells and apoptosis after spinal cord injury in rats [60]. |
| | Fisetin | (i) Exhibited antibacterial effect [61].
(ii) Protected cultured rat liver epithelial-like cells against AFB-1-induced cytotoxicity and inhibited the binding of [3] AFB-1 to cellular DNA [62].
(iii) Exhibited a predilection to inhibit histamine release stimulated by IgE-dependent ligands (antigen, anti-IgE, and con A) [63].
(iv) Inhibited TPA-caused epidermal ornithine decarboxylase induction and tumor promotion in relation to lipoxygenase inhibition [64].
(v) Inhibited PKC, almost 100% inhibition at a concentration of 100 micro-M from rat brain [65].
(vi) Suppressed mutagenesis in Salmonella typhimurium strain TA100 NR induced by direct-acting carcinogen N-methyl-N′-nitro-N-nitrosoguanidine [66].
(vii) Showed topoisomerase II dependent DNA cleavage activity [67].
(viii) Inhibited platelet aggregation [68].
Attenuated NO production in C6 astrocyte cell [69].
(ix) Blocked glucose uptake in myelocytic U937 cells [70].
(x) Inhibited corneal neovascularization; corneal blood vessels were induced by intrastromal implantation of pellets containing bFGF [71].
(xi) Inhibited the proliferation of HSC-T6 cells, hepatic stellate cells stimulated by serum, MCM, and PDGF [72].
(xii) Inducted apoptosis through activation of caspase-3 cascade and alternative expression of p21 protein in hepatocellular carcinoma cells SK-HEP-1 [73].
(xiii) Exhibited antiviral activities against IHNV and VHSV [31].
(xiv) Inhibited IL-4 and IL-13 synthesis and production by allergen- or anti-IgE-antibody-stimulated basophils [74].
(xv) Protected against hepatosteatosis in mice by inhibiting miR-378 [75].
(xvi) Protected bone by repressing NF-κB and MKP-1-dependent signaling pathways in osteoclasts [76].
(xvii) Enhanced behavioral performances and attenuated reactive gliosis and inflammation during aluminum chloride-induced neurotoxicity [77].
(xviii) Recuperated antioxidant status and protected hepatocellular ultrastructure from hyperglycemia mediated oxidative stress in STZ-induced rats diabetes model [78]. |
| | Kaempferol | (i) Inhibited estrogen binding to serum alpha-fetoprotein AFP in fetal or neonatal rats [79].
(ii) Showed antioxidative activity against metal-induced lipid peroxidation [80].
(iii) Suppressed TNF-α-stimulated E-selectin expression on HUVECs [81].
(iv) Exhibited high inhibitory potencies for the 20alpha-HSD activity on liver cytosol of male mice [82].
(v) Inhibited IgE or PMACI-mediated histamine release in RBL-2H3 cells and inhibited elevation of intracellular calcium [83]. |
| | Fustin | (i) Exerted inhibition of cell proliferation on Molt-4 cell and normal lymphocyte and enhanced IL-2 level [84].
(ii) Suppressed 6-OHDA-induced cell death, blocked 6-OHDA-induced increases in ROS, [Ca(2+)](i), Bax/Bcl-2 ratio, caspase-3 activity, and p38 phosphorylation [34].
(iii) Attenuated Abeta(1–42)-impaired learning [85].
(iv) Displayed antiviral activities against IHNV and VHSV [31]. |
| | Sulfuretin | (i) Exhibited potent antioxidants in a DPPH free radical scavenging assay [86].
(ii) Exhibited aldose reductase and advanced glycation end-products inhibition [57].
(iii) Inhibited iNOS and COX-2 protein and mRNA expression and reduced iNOS-derived NO, COX-derived PGE2, TNF-α, and IL-1β production in LPS-stimulated RAW264.7 and murine peritoneal macrophages [21].
(iv) Reduced cytokine (IL-1 β- and IFN-γ-) induced NF-κB activation, iNOS expression, and NO production in rat insulinoma RINm5F cells, and prevented STZ-induced hyperglycemia and hypoinsulinemia by suppression of NF-κB activation [87].
(v) Inhibited NF-κB pathway, suppressed the production of various cytokines in bronchoalveolar fluid and mucin production, and prevented the development of airway hyperresponsiveness on an ovalbumin-induced airway inflammation model in mice [88].
(vi) Induced apoptosis through activation of Fas, caspase-8, and the mitochondrial death pathway in HL-60 human leukemia cells [89].
(vii) Blocked NF-κB pathway in rheumatoid joints and reduced inflammatory responses and joint destruction [90].
(viii) Inhibited TPA-induced NF-κB activation, MMP-9 expression, and cell invasion in MCF-7 cells [91].
(ix)Induced miR-30C, downregulated cyclins D1 and D2, and triggered cell death in human cancer cell [92]. |
| | Quercetin | (i) Induced apoptosis in colorectal tumor cells via EGF receptor signaling [93].
(ii) Showed antioxidative activity against metal-induced lipid peroxidation [80].
(iii) Induced glutathione S-transferase and increased the resistance of cells to hydrogen peroxide [94].
(iv) Inhibited the proliferation of HSC-T6 cells and hepatic stellate cells stimulated by serum, MCM, and PDGF [72].
(v) Inhibited the antigen-IgE-mediated TNF-α and IL-4 production from RBL-2H3 [95].
(vi) Decreased the amount of myelin phagocytosed by a macrophage cell line [96].
(vii) Induced apoptosis through the activation of caspase-3 and caspase-8 in human leukemia U937 cells [97].
(viii) Inhibited Abeta fibril formation on neuronal HT22 murine neuroblastoma cells [98].
(ix) Inhibited prokaryotic SssI DNMT- and human DNMT1-mediated DNA methylation [99].
(x) Showed inhibitory effects against HSV-1 [100].
(xi) Exhibited inhibitory potencies for the 20alpha-HSD activity using liver cytosol of male mice [82].
(xii) Inhibited EGF-induced cell transformation of mouse epidermal JB6 Cl 41 cells [101].
(xiii) Inhibited tumor invasion via suppressing PKC Δ/ERK/AP-1-dependent MMP-9 activation in breast carcinoma cells [102].
(xiv) Inhibited the cell proliferation induced by 17-beta-estradiol in the E-screen assay (the evaluation of antiestrogenicity) [103]. |
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