Jin Shao,Tong Zhao,Hui-Ping Ma,Zheng-Ping Jia,Lin-Lin Jing
It was reported that 8-hydroxygenistein (8-OHG) was synthesized by methylation, bromination, methoxylation, and demethylation using cheap and readily available biochanin A as raw material. All synthesized products were structurally confirmed by ultra-high-performance liquid chromatography (UHPLC), infrared spectroscopy, mass spectrometry, 1H-nuclear magnetic resonance (NMR), and 13C-NMR. In addition, we examined the antioxidant capacity of 8-OHG using 6 different methods such as 1,1-diphenyl-2-picrylhydrazyl radical scavenging, 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonate) radical (ABTS) scavenging, nitric oxide radical (NO) scavenging, superoxide radical (O2 −•) scavenging, reducing power assay, and total antioxidant activity using ascorbic acid (VC) as a positive control. Compared with VC, 8-OHG exhibited higher total antioxidant activity and stronger scavenging activity on ABTS, NO, and O2 −•. These results indicate that 8-OHG is an excellent antioxidant agent and may be effective in preventing damage induced by free radical.
Junhua Ding,Jinggang Wang,Weihong Cao,Huajun Zheng,Zhenghong Guo,Zhengping Fang,Peng Chen,Juan Li
A bio-based phosphonate 4-(7-((diphenylphosphoryl)oxy)-5-hydroxy-4-oxo-4H-chromen-3-yl)phenyl diphenylphosphinate (DPGE) was synthesized using diphenylphosphinic chloride and genistein. DPGE was used to modify the flame retardancy of poly(ethylene 2,5-furandicarboxylate-co-ethylene terephthalate) (PEFT20) containing 20 mol % 2,5-furandicarboxylic acid. PEFT20 containing 8 wt % DPGE displays a UL-94 V0 rating and a limiting oxygen index of 29.8 vol %. The flame retardant mode is the comprehensive effects of melting-away, gas phase, and condensed phase induced by DPGE. In addition, triglycidyl isocyanurate (TGIC) was incorporated to regulate the mechanical performance of PEFT20/DPGE. The flexural and impact strengths of PEFT20/DPGE are modified greatly. The coupling reactions between PEFT20 and TGIC increase the molecular weight and mechanical properties of PEFT20 blends. But, TGIC counteracts the melting-away effect caused by DPGE. Therefore, too much TGIC causes the decrease in flame retardancy.
Background Temporomandibular disorder (TMD) pain is more prevalent in females than in males, with high estrogen levels potentially being a risk factor. Research indicates that 17β-estradiol (E2) exacerbates experimental occlusal interference (EOI)-induced orofacial hyperalgesia, which can be reversed by genistein. This study aimed to explore the central mechanisms within the spinal trigeminal nucleus (Sp5) related to the pain-exacerbating effect of E2 and the antiestrogenic properties of genistein in a model of EOI-induced chronic masseter pain. Methods Female rats underwent ovariectomy (OVX), followed by pretreatment with genistein or genistin (a control drug for genistein that does not inhibit protein tyrosine kinases (PTKs)), E2 replacement, and EOI application. The head withdrawal thresholds (HWTs) of the bilateral masseters were measured to evaluate pain sensitivity. Expression levels of p-ERK and two PTKs (Yes-associated protein, YAP; Src kinase, Src) in bilateral Sp5 were assessed through immunofluorescent staining and/or Western blotting. The ERK inhibitor PD98059 or vehicle was administered via intrathecal injection (i.t.) to inhibit the ERK1/2 signaling pathway. Results E2 intensified EOI-induced masseter mechanical hyperalgesia in OVX rats, and upregulated the phosphorylation of ERK1/2 in bilateral Sp5. Blocking phosphorylation of ERK1/2 in Sp5 reversed the exacerbating effect of E2. Genistein partially reversed the masseter hyperalgesia induced by E2 combined with EOI, possibly through the inhibition of PTKs and p-ERK1/2 upregulation in bilateral Sp5. Conclusion Genistein alleviates the pain-exacerbating effect of E2 on EOI-induced chronic mechanical hyperalgesia by inhibiting YAP and Src tyrosine kinases as well as the downstream ERK1/2 signaling pathway in Sp5.
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