4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮对聚氯乙烯上细菌生物膜的影响

目的观察4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮对聚氯乙烯表面表皮葡萄球菌形成的影响。方法用4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮覆盖在聚氯乙烯表面，通过体外生物膜形成实验，观察4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮对表皮葡萄球菌生物膜形成的影响。结果经4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮处理过的聚氯乙烯表面表皮葡萄球菌生物膜厚度和菌落数量少于对照组（P〈O．05）。结论4-溴-5-（4-甲氧苯基）-3-（甲氨基）-呋喃酮抑制聚氯乙烯上表皮葡萄球菌生物膜的形成。     

Potent mutagenicity in the Ames test of 2‐cyano‐4‐nitroaniline and 2,6‐dicyano‐4‐nitroaniline,components of disperse dyes

Genotoxicity data on commercial azo dyes and their components remain sparse, despite their widespread use. We have tested the mutagenicity of 2‐cyano‐4‐nitroaniline (CNNA) and 2,6‐dicyano‐4‐nitroaniline (CNCNNA), components of azo dyes such as Disperse Blue 165 and Disperse Red 73, in Ames test strains. Both compounds are extraordinarily potent frameshift mutagens, with much greater activity than structurally similar dihalonitroanilines and halodinitroanilines. Analysis of the responses of strains over‐expressing or deficient in bioactivation enzymes shows that bacterial nitroreductase and acetyl CoA: arylamine N‐acetyltransferase are important mediators of the mutagenicity of CNNA and CNCNNA. Environ. Mol. Mutagen. 57:10–16, 2016. © 2015 Wiley Periodicals, Inc.     

Mutagenic and clastogenic properties of 3-chloro-4-(dichloromethyl)-5-hydroxy-2 (5H)-furanone: a potent bacterial mutagen in drinking water

3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) was found to be a direct-acting mutagen in the Ames test for strains TA1535, TA1538, TA92, TA97, TA98, TA100 and TA102. The highest mutagenic response (approximately 13,000 revertants/nmol) was seen in strain TA100. The TA100 response was six- to tenfold higher than in TA98, TA97, and TA102, and 100- to 500-fold higher than in TA1535, TA92, and TA1538. The addition of a 9,000 x g supernatant fraction (S-9) from livers of polychlorinated biphenyl-treated rats, along with cofactors for NADPH generation, resulted in a 90% reduction in the TA100 mutagenicity. MX induced chromosomal aberrations in Chinese hamster ovary cells after 6-8 hr exposure without S-9 at a dose as low as 4 micrograms/ml, and after 2 hr exposure with S-9 at a dose of 75 micrograms/ml. The oral dose of MX lethal to 50% (LD50) in Swiss-Webster mice was determined to be 128 mg/kg. MX did not induce micronuclei in mouse bone marrow when administered by oral gavage at doses up to 70% of the LD50.     

Liquid-crystalline polymers containing heterocycloalkanediyl groups as mesogens, 6. Liquid-crystalline poly[trans-11-{4-[5-(4-methoxyphenyl)-1,3-dioxan-2-yl]-2,6-dimethylphenoxy}undecyl methacrylate] and poly[trans-11-{4-[5-(4-methoxyphenyl)-1,3-dioxan-2-yl]-2,6-dimethylphenoxy}undecyl acrylate]

The synthesis and characterization of poly[trans-11-{4-[5-(4-methoxyphenyl)-1,3-dioxan-2-yl]-2,6-dimethylphenoxy}undecyl methacrylate] and poly[trans-11-{4-[5-(4-methoxyphenyl)-1,3-dioxan-2-yl]-2,6-dimethylphenoxy}undecyl acrylate] is presented. Both polymers exhibit nematic mesophases and do not present side-chain crystallization. At temperatures higher than 160°C the 1,3-dioxane-2,5-diyl groups undergo a thermally induced trans-cis isomerization. A radical mechanism is proposed for this isomerization.     

Analysis of the genotoxicity of anthraquinone dyes in the mouse lymphoma assay

Despite their widespread use and potential for significant human exposure, genotoxicity data on anthraquinones and other dyes are limited. In this study, 16 anthraquinones and one azo dye (Solvent Red 1) were selected for testing using the thymidine kinase (tk) locus and micronucleus (MN) analysis in L5178Y/TK(+/-)-3.7.2C mouse lymphoma cells. Six of the dyes were from the same lot used in the NTP rodent bioassay. The dyes used were all production lots and thus varied in their purity. Disperse Blue 7, 2-aminoanthraquinone, 1-amino-2-methylanthraquinone, Disperse Blue 3 and Disperse Red 11 were genotoxic (inducing 1814 mutants/10(6) survivors, 369 MN/1000 cells at 13% survival; 397 mutants/10(6) survivors, 196 MN/1000 cells at 21% survival; 178 mutants/10(6) survivors, 119 MN/1000 cells at 51% survival; 264 mutants/10(6) survivors, 109 MN/1000 cells at 15% survival, respectively). Reactive Blue 19 was weakly mutagenic (inducing 144 mutants/10(6) survivors, but only 8 MN/1000 cells at 13% survival). Vat Yellow 4 and Solvent Red 1, with exogenous activation, were also mutagenic (inducing 300 mutants/10(6) survivors, 18 MN/1000 cells at 57% survival, and 100 mutants/10(6) survivors and 16 MN/1000 cells at 22% survival, respectively). With activation 1-nitro-2-methylanthraquinone was judged to give an equivocal mutagenicity response. The maximum test concentration was limited for some compounds by their solubility. Those chemicals that did not induce mutation or cytotoxicity at the limits of solubility were classified separately. Compounds which were not evaluated without exogenous activation because of insolubility but were evaluated with activation include 1-nitro-2-methylanthraquinone, Solvent Red 1 and Vat Yellow 4. Compounds which were not evaluated either with or without S9 activation because of their insolubility in the culture medium include 1-amino-2,4-dibromoanthraquinone, D&C Green, Disperse Blue 1, Disperse Red 60, Vat Blue 4, Vat Blue 20, Vat Brown 1 and Vat Brown 3.     

Salmonella typhimurium (TA100) mutagenicity of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone and its open- and closed-ring analogs

The mutagenicities of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX, compound 1), 3-chloro-4-(dichloromethyl)-2(5H)-furanone (RMX, compound 6), and 2-(dichloromethyl)-3,3-dichloropropenal (TCB, compound 7) were determined in the same assay and in repetitive determinations using Salmonella typhimurium (TA 100) without microsomal fraction activation. In addition, the mutagenicity of 2-methyl-3,3-dichloropropenal (compound 8) was assayed in the same manner although not simultaneously with MX, RMX, and TCB. This study was undertaken to ascertain the role of open- and closed-ring forms of MX in the mutagenicity of MX. MX proved to be roughly 100 times more mutagenic than the open-ring analogue TCB and 10 times more mutagenic than the closed-ring analogue RMX. Compound 8 was inactive. Assay stability of the three active compounds in Vogel-Bonner medium at 38 degrees C was estimated as the chemical half-life values by following the change in UV absorbance at selected wave lengths. Half-life values were 10.7, 2.6, and 2.8 hr, respectively, for MX, RMX, and TCB. The enhanced mutagenicity of MX relative to RMX and TCB is attributed to the intrinsic mutagenicity of MX and its greater stability is judged to play only a minor role. Moreover, the greater mutagenicity of the closed-ring analogue RMX relative to the open-ring analogue TCB points to the ring form of MX as the active species even though the open form of MX is predominant under assay conditions.     

Mutation spectra of the drinking water mutagen 3-chloro-4-methyl-5-hydroxy-2(5H)-furanone (MCF) in Salmonella TA100 and TA104: comparison to MX

The chlorinated drinking water mutagen 3-chloro-4-methyl-5-hydroxy-2(5H)-furanone (MCF) occurs at concentrations similar to or greater than that of the related furanone 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX). MCF and MX differ structurally only by replacement of a 3-methyl in MCF with a 3-dichloromethyl in MX; yet, MCF is significantly less mutagenic than MX and produces different adducts when reacted with nucleosides or DNA. To explore further the effects that these structural differences might have on the biological activity of MCF and MX, we determined the mutation spectra of MCF in Salmonella strains TA100 and TA104 and of MX in strain TA104; the spectrum of MX in TA100 had been determined previously. In TA100, which presents only GC targets for mutagenesis, MCF induced primarily (75%) GC --> TA transversions, with most of the remaining revertants (20%) being GC --> AT transitions. This spectrum was not significantly different from that of MX in TA100 (P = 0.07). In TA104, which presents both GC and AT targets, MCF induced a lower percentage (57%) of GC --> TA transversions, with most of the remaining revertants (33%) being AT --> TA transversions. In contrast, MX induced almost only (98%) GC --> TA transversions in TA104, with the remaining revertants (2%) being AT --> TA transversions. Thus, almost all (98%) of the MX mutations were targeted at GC sites in TA104, whereas only 63% of the MCF mutations were so targeted. These results are consistent with the published findings that MX: (1) forms an adduct on guanosine when reacted with guanosine, (2) induces apurinic sites in DNA, and (3) forms a minor adduct on adenosine when reacted with adenosine or DNA. The results are also consistent with evidence that MCF forms adenosine adducts when reacted with adenosine. Our results show that the replacement of the 4-methyl in MCF with a 4-dichloromethyl to form MX not only increases dramatically the mutagenic potency but also shifts significantly the mutagenic specificity from almost equal targeting of GC and AT sites by MCF to almost exclusive targeting of GC sites by MX. Environ. Mol. Mutagen. 35:106-113, 2000 Published 2000 Wiley-Liss, Inc.     

(9-[4-acetyl-3-hydroxy-2-n-propylphenoxy) methyl]-3-(1H-tetrazol-5-yl)-4H-pyrido [1,2-a] pyrimidin-4-one), AS-35, inhibits leukotriene synthesis

AS-35, (9-[4-acetyl-3-hydroxy-2-n-propylphenoxy) methyl]-3-(1H-tetrazol-5-yl)-4H-pyrido[1, 2-a] pyrimidin-4-one), was developed as a leukotriene (LT) receptor antagonist, which also inhibited IgE-mediated release of leukotrienes (LTs). We have investigated the action of AS-35 on the enzyme activities which are involved in the synthesis of LTC(4) and LTB(4) (LT-synthesizing enzymes); cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LO), leukotriene (LT)C(4) synthase and LTA(4) hydrolase. AS-35 dose-dependently inhibited IgE- and A23187-stimulated production of LTC(4) by up to 71.5-84.8% and that of LTB(4) by 48.3-49.2% at 2. 5x10(-5) M. The assays for cPLA(2)(-), 5-LO-, LTC(4) synthase- and LTA(4) hydrolase-activities revealed that the inhibition is attributable to suppression of cPLA(2), 5-LO and LTC(4) synthase but not LTA(4) hydrolase. We have also studied the action of AS-35 on the release of beta-hexosaminidase (beta-HEX) as a marker of preformed mediators. AS-35 had only weak inhibitory action on the release of beta-HEX. The results indicate that anti-allergic action of AS-35 is predominantly attributable to its inhibition of LT synthesis by suppressing three consecutive enzymes for LTC(4) synthesis.     

Functional polymers, 11. Synthesis and polymerization of 2-(2-hydroxy-5-vinylphenyl)-2 H-benzotriazole

2-(2-Hydroxy-5-vinylphenyl)-2H-benzotriazole ( 9 ) was prepared by a seven step synthesis in about a 25% overall yield starting from o-nitroaniline. Diazotization in aqueous HCl gave a diazonium salt which was coupled with p-ethylphenol to an azo-dye which was reduced with zinc powder in sodium hydroxide solution to 2-(2-hydroxy-5-ethylphenyl)-2H-benzotriazole ( 4 ). This compound was acetylated and then brominated with N-bromosuccinimide to 2-[2-acetoxy-5-(1-bromoethyl)phenyl]-2H-benzotriazole ( 6 ) which was dehydrobrominated with triethylamine in acetonitrile or tributylamine in dimethylacetamide to the vinyl compound which was hydrolyzed to 9 . This monomer was readily homopolymerized and copolymerized with styrene and methyl methacrylate using 2,2′-azobis(2-methylpropionitrile) as initiator.     

Liquid crystal polymers containing macroheterocyclic ligands, 7. Synthesis and characterization of 4-[(4-methacryloyloxy)-undecyloxy-2-methylphenylethynyl]phenyl (benzo-15-crown-5)-4′-carboxylate

The synthesis and thermal characterization of 4-[(4-methacryloyloxy)undecyloxy-2-methyl-phenylethynyl]phenyl (benzo-15-crown-5)-4′-carboxylate ( 8 ) and of poly( 8 ) are described. 8 exhibits monotropic nematic and smectic mesophases, while poly( 8 ) shows enantiotropic nematic and smectic mesophases. In spite of its very long flexible spacer, poly( 8 ) does not display sidechain crystallization.     

Baclofen antagonism by 4-amino-3-(5-methoxybenzo[b]furan-2-yl) butanoic acid in the cat spinal cord

When administered microelectrophoretically, 4-amino-3-(5-methoxybenzo[b]furan-2-yl)butanoic acid (MBFG) reversibly reduced the presynaptic depression by (−)-baclofen of the monosynaptic excitation of spinal interneurones by impulses in muscle low-threshold afferent fibres of the cat as well as the postsynaptic depression by (−)-baclofen of the firing of these neurones. MBFG, as an antagonist of (−)-baclofen, may be useful in investigating the structure-activity relationships of central and peripheral baclofen receptors.     

Induction of gastrointestinal tract nuclear anomalies in B6C3F1 mice by 3-chloro-4-(dichloromethyl)-5-hydroxy-2[5H]-furanone and 3,4-(dichloro)-5-hydroxy-2[5H]-furanone, mutagenic byproducts of chlorine disinfection

Two chlorinated hydroxylated furanones, 3-chloro-4-(dichloromethyl)-5-hydroxy-2[5H]-furanone (MX) and 3,4-(dichloro)-5-hydroxy-2[5H]-furanone (MA), are bacterial mutagens and they are also byproducts of chlorine disinfection, and frequent contaminants of drinking water. In this work MX is shown to induce nuclear anomalies in the gastrointestinal tract of the B6C3F1 mouse. The other chlorohydroxy-furanone, MA, gives suggestive evidence of activity. In this bioassay MX was approximately equivalent in potency to epichlorohydrin (ECH) but was much less potent than methylnitrosourea (MNU). The latter two chemicals are confirmed rodent gastrointestinal tract carcinogens. The duodenum was the most sensitive tissue responding with both increased numbers of nuclear anomalies per mouse and increased incidence of animals presenting the nuclear aberrations 24 hr after a single oral dose of 0.37 mmol/kg-1 of MX. MA also induced a significant increase in duodenal nuclear anomalies, but only at the highest dose (0.46 mmol/kg-1). The proximal colon and forestomach responded to MX but not MA. This is the first study demonstrating that chlorohydroxyfuranones are capable of inducing nuclear toxicity in vivo. However, it is clear, for MX at least, that its potency in the gastrointestinal tract nuclear anomalies assay is not commensurate with its extreme bacterial mutagenicity. Since the gastrointestinal tract tissues are directly exposed to orally administered genotoxins, one possible explanation for the weak response observed in this study could be that mammalian cells can effectively detoxify chlorohydroxyfuranones.     

Immunomodulatory effect of a newly synthesized compound, TOK-8801 (N-(2-phenylethyl)-3,6,6-trimethyl-5,6-dihydroimidazo [2,1-b]thiazole-2-carboxamide) on antibody production in vivo and delayed-type hypersensitivity in mice

The immunopharmacological effects of a newly synthesized compound in vivo, TOK-8801 (N-(2-phenylethyl)-3,6,6-trimethyl-5,6-dihydroimidazo[2,1-b]thi azo le-2- carboxamide), on the anti-SRBC plaque-forming cell (PFC) response and delayed-type hypersensitivity (DTH) reaction were investigated. Oral administration of TOK-8801 (0.1-10 mg/kg) resulted in the suppression of the PFC responses to varying doses of antigen (5 x 10(6), 2 x 10(7), 1 x 10(8)) in C3H/He strain mice (7 W) which are high responders to SRBC antigen. On the other hand, the compound augmented the PFC response in aged mice (8-9 months) in which the PFC response was markedly depressed compared with that in young mice. In the experiment of the methylated human serum albumin-induced DTH reaction, TOK-8801 augmented the reaction in low responder (C57BL/6) mice by oral administrations of 0.1-1 mg/kg for 5 days from the sensitization, whereas suppressed the reaction in high responder (ICR) mice. These immunopharmacological actions of TOK-8801 were compared in dose and activity with those of lobenzarit and bucillamine. Thus, these results suggest that TOK-8801 may act as an immunomodulating agent and would be expected to be a useful agent for autoimmune diseases such as rheumatoid arthritis.     

Quantitative analysis of Z-2-[4-(4-chloro-1,2-diphenyl-but-1-enyl)phenoxy]ethanol in human plasma using high-performance liquid chromatography

A highly sensitive and precise high-performance liquid chromatography (HPLC) assay was developed and validated for the quantitation of Z-2-[4-(4-chloro-1,2-diphenyl-but-1-enyl) phenoxy]ethanol (FC-1271a) in human plasma. Plasma samples (1.0 ml) containing FC-1271a and internal standard (toremifene citrate; Farestono) were extracted using a 2% 1-butanol, 98% hexane solution with an extraction efficiency of >97%. Samples were reconstituted in methanol, irradiated with high intensity ultraviolet light (254 nm) for 1 min, and injected onto a C18 reverse phase column. Samples were eluted isocratically at a flow-rate of 0.5 ml/min with a mobile phase consisting of 6.5% water and 0.5% triethylamine in methanol. The fluorescence of photochemically activated compounds was detected using a fluorometer set at an excitation wavelength of 266 nm and emission wavelength of 370 nm. Under these assay conditions, standard calibration curves were linear through a concentration range of 10-400 ng/ml. In summary, we have developed and validated an HPLC assay to quantitate FC-1271a in human plasma.     

3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone [MX] shows initiating and promoting activities in a two-stage BALB/c 3T3 cell transformation assay

A transformation assay using BALB/c 3T3 cells was conducted on 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) to assess initiation and promotion activities of MX carcinogenesis. Statistically significant positive responses were obtained compared with the corresponding solvent controls in both the initiation assay post-treated with 12-O-tetradecanoylphorbol 13-acetate (TPA) and the promotion assay pretreated with 3-methylcholanthrene (MCA). Both TPA and MX inhibited metabolic cooperation in an assay using co-culture of V79 6-thioguanine (6-TG) sensitive and insensitive cells. However, cells isolated from transformed foci in the initiation assay did not induce any nodules after inoculation to BALB/c mice, the strain of mouse from which the transformation assay cells were derived. Although the study was carried out for 2-3 weeks, this might have been too short to develop nodules under the conditions of this experiment. This in vitro cell transformation study with MX adds supportive information to studies showing MX carcinogenicity and tumour promoter activity, and adds mechanistic understanding of the action of MX.     

Preparation of 5-hydroxy-7-methoxy-2,2-dimethyl-6-octyl(and 8-octyl)-4-chromanones and their Properties as UV Absorbers

5-Hydroxy-7-methoxy-2,2-dimethyl-6-octyl(and 8-octyl)-4-chromanones ( 2a and 2b ) were synthesized via 5,7 dihydroxy-2,2-dimethyl-6-octyl (and 8-octyl)-4-chromanones ( 1a and 1b ) from phloroglucinol as a starting material. Cyclohexane solutions of 1a, 1b, 2a , and 2b were irradiated. The photostability of 2a and 2b was found to be better than that of 1a and 1b . Poly(vinyl chloride) film containing 6, 7 wt.-% of 2b was found to be most stable against photooxidation.     

Pharmacological properties of the hydroxylated histamine, (±)-4(5)-(2-amino-1-hydroxyethyl)-imidazole

The pharmacological effects of the -hydroxylated histamine, 4(5)-(2-amino-1-hydroxyethyl)-imidazole, on smooth muscle contraction of the ileum (H₁-receptor activity) and gastric acid secretion (H₂-receptor activity) of the guinea-pig were investigated and compared with those of histamine. Although -hydroxy histamine contracted the ileum with the same maximal response as hstamine, the concentration response curve was shifted to the right by approximately three orders of magnitude. At submaximal concentrations, co-administration of -hydroxy histamine with histamine revealed only additive effects. This H₁-activity was competitively inhibited by diphenhydramine. Similarly, the hydroxylated analogue also increased intracellular cyclic AMP level and [¹⁴C] aminopyrine accumulation as a marker of acid secretion in the parietal cells. However, the EC₅₀ was approximately ten fold that of histamine. This H₂-receptor activity was inhibited completely by cimetidine. These results suggest that -hydroxy histamine possesses nearly full intrinsic activities at both H₁ and H₂-receptors and that the introduction of a hydroxyl group at the -carbon reduces and dissociates these activities.     

Side-chain liquid-crystalline polysalts. Synthesis and thermal properties of poly{1-[ω-(4′-methoxy-4-biphenylyloxy)alkyl]-4-vinylpyridinium bromide} or poly[1-(2-{2-[2-(4′-methoxy-4-biphenylyloxy)ethoxy]ethoxy}ethyl)-4-vinylpyridinium bromide]

The synthesis and thermal properties of a new type of side-chain liquid-crystalline polymers, incorporating ionic groups, are described. The polymers are obtained upon spontaneous polymerization (simultaneous quaternization and polymerization) of 4-vinylpyridine in the presence of ω-(4′-methoxy-4-biphenylyloxy)alkyl or 2-{2-[2-(4′-methoxy-4-biphenylyloxy)ethoxy]ethoxy}-ethyl bromide. Fully quaternized polymers of high molecular weight are obtained. As the analogous low-molecular-weight molecules previously studied these polymers form smectic mesophases, although the mesogenic groups, which include the pyridinium rings, are directly connected to the polyvinylic backbone.     

Prevention of in vitro and in vivo acute ischemic neuronal damage by (2S)-1-(4-amino-2,3,5-trimethylphenoxy)-3-{4-[4-(4-fluorobenzyl) phenyl]-1-piperazinyl}-2-propanol dimethanesulfonate (SUN N8075), a novel neuroprotective agent with antioxidant properties

(2S)-1-(4-Amino-2,3,5-trimethylphenoxy)-3-{4-[4-(4-fluorobenzyl) phenyl]-1-piperazinyl}-2-propanol dimethanesulfonate (SUN N8075) is a novel antioxidant with neuroprotective properties. We examined whether SUN N8075 inhibited the neuronal damage resulting from permanent focal cerebral ischemia, and examined its neuroprotective properties in vivo and in vitro mechanism. Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion in mice, and the resulting infarction, brain swelling, and neurological deficits were evaluated after 24 h or 72 h. Brain damage was assessed histochemically using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and antibody recognizing 4-hydroxynonenal histidine adduct (4-HNE). In the in vitro study, we examined the effects of SUN N8075 on 1) lipid peroxidation in mouse brain homogenates and 2) cell viability and caspase-3 protease activity under a hypoxic insult or FeSO(4) in rat cultured cerebrocortical neurons. SUN N8075 administered either 10 min before or at 1 h after the occlusion reduced both infarction size and neurological deficits. SUN N8075 reduced brain swelling when administered 10 min before, 1 h, or 3 h after occlusion. Furthermore, only pretreatment (administered 10 min before) decreased infarct volume and brain swelling at 72 h after middle cerebral artery occlusion. SUN N8075 reduced the number of TUNEL-positive cells and decreased the level of oxidative damage, as assessed by immunopositive staining to 4-HNE. SUN N8075 inhibited lipid peroxidation, leakage of lactate dehydrogenase, caspase-3 activation induced by in vitro hypoxia, and the neuronal damage induced by in vitro FeSO(4) exposure. These findings indicate that SUN N8075 has neuroprotective effects against acute ischemic neuronal damage in mice and may prove promising as a therapeutic drug for stroke.