Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathy via PI3K/Akt pathway

BACKGROUND Development of end-stage renal disease is predominantly attributed to diabetic nephropathy(DN).Previous studies have indicated that myricetin possesses the potential to mitigate the pathological alterations observed in renal tissue.Never-theless,the precise molecular mechanism through which myricetin influences the progression of DN remains uncertain.AIM To investigate the effects of myricetin on DN and explore its potential therapeutic mechanism.METHODS Db/db mice were administered myricetin intragastrically on a daily basis at doses of 50 mg/kg or 100 mg/kg for a duration of 12 wk.Subsequently,blood and urine indexes were assessed,along with examination of renal tissue pathology.Kidney morphology and fibrosis were evaluated using various staining techniques including hematoxylin and eosin,periodic acid–Schiff,Masson’s trichrome,and Sirius-red.Additionally,high-glucose culturing was conducted on the RAW 264.7 cell line,treated with 25 mM myricetin or co-administered with the PI3K/Akt inhibitor LY294002 for a period of 24 h.In both in vivo and in vitro settings,quantification of inflammation factor levels was conducted using western blotting,real-time qPCR and ELISA.RESULTS In db/db mice,administration of myricetin led to a mitigating effect on DN-induced renal dysfunction and fibrosis.Notably,we observed a significant reduction in expressions of the kidney injury markers kidney injury molecule-1 and neutrophil gelatinase associated lipocalin,along with a decrease in expressions of inflammatory cytokine-related factors.Furthermore,myricetin treatment effectively inhibited the up-regulation of tumor necrosis factor-alpha,interleukin-6,and interluekin-1βinduced by high glucose in RAW 264.7 cells.Additionally,myricetin modulated the M1-type polarization of the RAW 264.7 cells.Molecular docking and bioinformatic analyses revealed Akt as the target of myricetin.The protective effect of myricetin was nullified upon blocking the polarization of RAW 264.7 via inhibition of PI3K/Akt activation using LY294002.CONCLUSION This study demonstrated that myricetin effectively mitigates kidney injury in DN mice through the regulation of macrophage polarization via the PI3K/Akt signaling pathway.

Myricetin alleviates ovalbumin-induced allergic rhinitis in mice by regulating Th1/Th2 balance

Objective:To evaluate the effect of myricetin on ovalbumin(OVA)-induced allergic rhinitis in mice.Methods:Mice were sensitized and challenged using OVA(5%,500 mL)intraperitoneally and intranasally,respectively,on an alternative day for 14 days,followed by administration of myricetin(50,100,and 200 mg/kg)till day 21.Nasal symptoms,biochemical parameters,protein expressions,and histopathology were observed.Results:OVA-induced increased nasal symptoms including rubbing,sneezing,and discharge were significantly reduced by myricetin(100and 200 mg/kg)(P<0.05).Myricetin also protected against histamine challenge and attenuated elevated serum immunoglobulin E(IgE;total and OVA-specific),total IgG1,andβ-hexosaminidase levels,as well as leukotriene C4 and interleukins levels in nasal lavage fluid(P<0.05).Western blot analysis showed that myricetin significantly upregulated the protein expression of T-box expressed in T cells,while downregulating the protein expression of GATA binding protein 3,NF-κB,and IκB-α(P<0.05).Additionally,OVA-induced histopathological abberations in the nasal mucosa was markedly ameliorated by myricetin treatment(P<0.05).Conclusions:Myricetin exerts anti-allergic effects against OVAinduced allergic rhinitis via regulating Th1/Th2 balance.

Recent advances in research on vine tea,a potential and functional herbal tea with dihydromyricetin and myricetin as major bioactive compounds

Vine tea has been used as an herbal tea by several ethnic minorities for hundreds of years in China.Flavonoids,a kind of indispensable component in a variety of nutraceutical,pharmaceutical and cosmetic applications,are identified to be the major metabolites and bioactive ingredients in vine tea.Interestingly,vine tea exhibits a wide range of significant bioactivities including anti-oxidant,anti-inflammatory,anti-tumor,antidiabetic,neuroprotective and other activities,but no toxicity.These bioactivities,to some extent,enrich the understanding about the role of vine tea in disease prevention and therapy.The health benefits of vine tea,particularly dihydromyricetin and myricetin,are widely investigated.However,there is currently no comprehensive review available on vine tea.Therefore,this report summarizes the most recent studies investigating bioactive constituents,pharmacological effects and possible mechanisms of vine tea,which will provide a better understanding about the health benefits and preclinical assessment of novel application of vine tea.

Safety Evaluation of Myricetin and Crude Extract from Myrica rubra Leaves on Non-target Organisms

[ Objective] The study aimed to supply important basis for developing environment-friendly pesticides with myricetin and crude extract of Myrica rubra leaves as effective components. [ Method] According to ＂Test guidelines for environmental safety evaluation on chemical pesticides＂, the toxicity of myricetin and crude extract of M. rubra leaves on non-target organisms was determined and the safety evaluation was carried out. [Result] MyriceUn and crude extract of M. rubra leaves had low toxicity on non-target organisms, such as earthworm, silkworm and soil microbes. Myricetin showed low toxicity and the crude extract of M. rubra leaves showed middle toxicity on tadpole. The high-concentration crude extract of M. rubra leaves had some antifeedant effect on silkworm. [ Conclusion] Myricetin and crude extract of M. rubra leaves had low toxicity on non-tar- get organisms in environment and they were relatively safe.

Highly sensitive simultaneous electrochemical determination of myricetin and rutin via solid phase extraction on a ternary Pt@r-GO@MWCNTs nanocomposite

The simultaneous electrochemical determination of myricetin and rutin remains a challenge due to their indistinguishable potentials.To solve this problem,we constructed a ternary platinum nanoparticle,reduced graphene oxide,multi-walled carbon nanotubes (Pt@r-GO@MWCNTs) nanocomposite via a facile one-pot synthetic method.Under the optimized conditions,the ternary Pt@r-GO@MWCNTs nanocomposite exhibited good electrocatalytic activity toward myricetin and rutin via solid phase extraction and excellent performance for the simultaneous determination of myricetin and rutin.The oxidation peak current of myricetin was proportional to its concentrations in the range of 0.05-50μM with a detection limit of 0.01μM (S/N=3).The linear range for rutin was 0.05-50μM with a detection limit of 0.005μM(S/N=3).The ternary nanocomposite sensor also exhibited good reproducibility and stability,and was successfully used for the simultaneous determination of myricetin and rutin in real orange juice samples with recoveries ranging between 100.57% and 108.46%.

Myricetin protects against lipopolysaccharide-induced disseminated intravascular coagulation by anti-inflammatory and anticoagulation effect

Objective: To explore the therapeutic effect and mechanism of myricctin on disseminated intravascular coagulation(DIC). Methods: The DIC model was established by injection of60 mg/kg LPS in KM mice, and the treatment groups were injected myricetin with different concentrations(25 or 50 mg/kg) 30 min before the model was established. Both coagulation indicators and organ function were tested, including PT, APTT, fibrinogen. AST, ALT. BUN and tissue section. In vitro, the inflammatory model of RAW 264.7 macrophage cells were established by 10 μg/mL LPS. The treatment group was treated with 50 μmol/mL myricetin for 30 min before LPS, and the expression of TNF-a and p-NF-KB was detected, further to explore the therapeutic mechanism. Results: LPS-induced DIC led to a reduction of fibrinogen and a rise of PT, APTT,AST, ALT, BUN levels, but the treatment of myricctin significantly inhibited these abnormalities. Histopathology analysis also revealed that myricetin remarkably protected the liver and renal damage. In vitro, the expression of TNF-α and p-NF-κB induced by LPS was repressed by myricetin. Conclusions: This study provides new insights into the protective effects of myricetin in LPS-induced DIC by anticoagulant and anti-inflammatory via suppressing the activation of p-NF-κB which decreased TNF-α level.

Minireview:Therapeutic potential of myricetin in diabetes mellitus

Epidemiological studies have demonstrated that diabetes mellitus(DM)is a serious health burden for both governments and healthcare providers.Myricetin,a natural flavonol with hydroxyl groups at 3,5,7,3′,4′and 5′positions,is commonly ingested through human diets such as fruits,vegetables,tea,berries and red wine.Although few epidemiological and clinical studies have reported the health benefits of myricetin on DM,increasing evidences from in vitro and animal studies have confirmed its hypoglycemic effect.Importantly,myricetin has the function to ameliorate insulin resistance.Moreover,myricetin can execute the functions including anti-inflammation,anti-oxidative stress,anti-aldose reductase,antinon-enzymatic glycation and anti-hyperlipidemia.All of these functions may provide the contribution to the prevention of DM and diabetic complications.In this article,a comprehensive discussion to address the potential benefits of myricetin on DM and its underlying mechanisms has been conducted.©2012 Production and hosting by Elsevier B.V.on behalf of Beijing Academy of Food Sciences.

Comparison of the Ability of Myricetin and Quercetin to Modulate the Oxidative DNA Damage Induced by Heterocyclic Amines

The aim of the present study was to compare the ability of the myricetin and quercetin to modulate the oxidative DNA damage induced by 2-amino-3, 8- dimethylimidazo [4,5-f] quinoxaline (8-MeIQx), 2-amino- 3, 4, 8- trimethylimidazo [4, 5-f]-quinoxaline (4,8-diMeIQx) and 2-amino-1-methyl-6-phenyl-imidazo [4,5-b] pyridine (PhIP), in human hepatoma cells. DNA damage (strand breaks and oxidized purines/pyrimidines) was evaluated by the alkaline single-cell gel electrophoresis or comet assay. None of the myricetin and quercetin concentrations tested protected against 8-MeIQx, 4, 8-diMeIQx and PhIP-induced DNA strand breaks. The oxidized pyrimidines induced by 4, 8-diMeIQx and PhIP were reduced by myricetin but not by quercetin. Quercetin reduced the oxidized purines induced by 8-MeIQx and PhIP, while myricetin also reduced the induced by 4, 8-diMeIQx. One feasible mechanism by which myricetin and quercetin exert their protective effect towards HCAs-induced oxidative DNA could be related in part to the reduction of human CYP1A1. Another mechanism claimed to be responsible for the protective effect of myricetin and quercetin is the induction of phase II metabolizing enzymes such as UDP-glucuronyltrasferase (UGT). The ethoxyresorufin O-deethylation (CYP1A1) activity was moderately inhibited by myricetin, while little effect was observed by quercetin. On the contrary, quercetin showed the greatest increase on UDP-glucuronyltransferase activity. However, these are not the only mechanisms by which myricetin and quercetin exert their protective effect, other mechanisms such as stimulation of the repair of carcinogen-induced DNA damage and or the free radical scavenging efficiency have been also implicated. In conclusion, our results clearly indicate that myricetin was more efficient than quercetin to prevent DNA damage (oxidized purines and pyrimidines) induced by the three HCAs evaluated. This protective effect depends on the chemical structure of flavonoid and the mutagen studied.

Myricetin protects hippocampal CA3 pyramidal neurons and improves learning and memory impairments in rats with Alzheimer's disease

There is currently no treatment for effectively slowing the progression of Alzheimer＇s disease, so early prevention is very important. Numerous studies have shown that flavonoids can improve memory impairment. The present study investigated the effects of myricetin, a member of the flavonoids, on intracerebroventricular streptozotocin induced neuronal loss and memory impairment in rat models of Alzheimer＇s disease. Myricetin at 5 or 10 mg/kg was intraperitoneally injected into rats over 21 days. Control rats were treated with 10 m L/kg saline. Behavioral test（the shuttle box test） was performed on day 22 to examine learning and memory in rats. Immediately after that, hematoxylin-eosin staining was performed to observe the morphological change in hippocampal CA3 pyramidal neurons. Myricetin greatly increased the number of hippocampal CA3 pyramidal neurons and improved learning and memory impairments in rats with Alzheimer＇s disease. These findings suggest that myricetin is beneficial for treatment of Alzheimer＇s disease.

Theoretical Investigation on the Relationship between the Structures and Antioxidant Activities of Myricetin and Dihydromyricetin

The geometry of myricetin and dihydromyricetin was optimized by DMol3 program based on DFT. The optimized structures have been proved to be stable by real frequencies obtained.The parameters of geometry optimization,vibration frequencies,atomic charges,thermodynamics,Fukui functions,and frontier molecular orbital had been obtained. The thermodynamic properties of 2 molecules were fitted and the relationship between the thermodynamic function and temperature was obtained. The correlation coefficient of the obtained equations is larger than 0.99,indicating that the function is approximately linear in the whole temperature range. The calculated results showed the O–H molecular structures were the main group affecting the antioxidant activity and the oxygen in the benzene ring is the electrophilic reaction site. Ortho-OH on the benzene formed intramolecular hydrogen bonds,which contributed to the stability of the benzene ring. It may be the active site for the occurrence of the reaction.

Myricetin and Hesperidin Inhibit Cerebral Thrombogenesis and Atherogenesis in <i>Apoe^-/-</i>and <i>Ldlr^-/-</i>Mice

Flavonoids have been reported to possess strong antioxidant activities that moderate endothelial dysfunction and demonstrate protective effects on cardiovascular disease. Our previous studies confirmed that flavonoids, including hesperidin, naringin and nobiletin, inhibited thrombogenesis and hypertension in stroke prone spontaneously hypertensive rats (SHRSP) by protecting the endothelium from the adverse effects of free radical formation. We have now further investigated the protective effects of myricetin and hesperidin on cerebral thrombosis and atherogenesis in apolipoprotein E (apoE) and lowdensity lipoprotein receptor (LDLR) deficient (Apoe-/- and Ldlr-/- double knockout) mice. Three groups of mice were fed high fat diet alone and high fat diet mixed with myricetin (100 mg/kg/day and 200 mg/kg/day) or glucosyl hesperidin (G-hesperidin;250 mg/kg/day and 500 mg/kg/day) for 8 weeks. There were no differences in body weight related to administration of the flavonoids. Thrombotic tendency was assessed using a He-Ne laser technique in the murine cerebral pial vessels. In addition, atherogenesis was quantified histologically after dissection of the aorta from each mouse and staining with Oil Red O solution. The percentages of stained area to whole area of dissected aorta were calculated as indices of anti-atherogenic activity. Both myricetin and G-hesperidin significantly inhibited thrombogenesis in vivo and significantly inhibited atherogenesis compared to control mice (p < 0.001). These findings demonstrated that daily intake of myricetin and hesperidin suppressed the development of atherogenesis and thrombogenesis, possibly associated with the potent antioxidant effects of the flavonoids.

Myricetin inhibits interferon-γ-induced programmed death ligand-1 and indoleamine 2,3-dioxygenase 1 expression in lung cancer cells

OBJECTIVE Programmed death ligand-1(PD-L1)and indoleamine 2,3-dioxygenase 1(IDO1)are immune checkpoints which can be induced by interferon-γ(IFN-γ)in the tumor microenvironment,leading to immune escape of tumors.Myricetin(MY)is a flavonoid distributed in many edible and medicinal plants.The aim of this study is to clarify the effect and the mechanism of MY on inhibiting IFN-γ-induced PD-L1 and IDO1 in lung cancer cells.METHODS Expressions of PD-L1 and major histocompatibility complex-I(MHC-I)were evaluated by flow cytometry and Western blotting,and the expression of IDO1 was measured by Western blotting.qRT-PCR was used to detect their mRNA levels.The function of T cells was evaluated using a co-culture system consist of lung cancer cells and the Jurkat-PD-1 T cell line that overexpressing PD-1.Molecular docking analysis,Western blotting and immunofluorescence were used for mechanism study.RESULTS MY potently inhibited IFN-γ-induced PD-L1 and IDO1 expression in human lung cancer cells,while didn't show obvious effect on the expression of MHC-I.In addition,MY restored the survival,proliferation,CD69 expression and interleukin-2(IL-2)secretion of Jurkat-PD-1 T cells suppressed by IFN-γ-treated lung cancer cells in the co-culture system.Mechanistically,IFN-γup-regulated PD-L1 and IDO1 at the transcriptional level through the JAK-STAT-IRF1 axis,which was targeted and inhibited by MY.CONCLUSION Our research revealed a new insight into the anti-tumor effects of MY which inhibited IFN-γ-induced PD-L1 and IDO1 expression,supporting the potential of MY in anti-tumor immunotherapy.

Molecular Docking Studies of Myricetin and Its Analogues against Human PDK-1 Kinase as Candidate Drugs for Cancer

Phosphoinositide-dependent protein kinase-1 (PDK1), the class of serine threonine kinase, is a master regulator of the AGC family of kinases. It is a main component of the PI3K pathway. As it is reported that this pathway is most commonly, and this pathway is the most commonly deregulated among many cancers. So designing a selective inhibitor of PDK1 may have the efficacy as an anticancer agent. Herein, we describe our work focused on the structure based on screening of 95% similar analogues of Myricetin deposited in PubChem database as earlier studies have been suggested that myricetin acts as an anti cancer agent. Further molecular docking as well as the in silico ADMET studies are incorporated on these compounds to evaluate the binding and pharmacokinetic properties of these compounds. Due to low oral bioavailability, clinical use of myricetin is limited. Therefore this study is an attempt towards screening of structurally similar better compounds as compare with myricetin which can act as better inhibitor against PDK-1.

Flavonoid Myricetin as Potent Anticancer Agent: A Possibility towards Development of Potential Anticancer Nutraceuticals

Good nutrition plays a crucial role in maintaining a balanced lifestyle. The beneficial effects of nutrition have been found to counteract nutritional disturbances with the expanded use of nutraceuticals to treat and manage cardiovascular diseases, cancer, and other developmental defects over the last decade. Flavonoids are found abundantly in plant-derived foods such as fruits, vegetables, tea, cocoa, and wine. Fruits and vegetables contain phytochemicals like flavonoids, phenolics, alkaloids, saponins, and terpenoids. Flavonoids can act as anti-inflammatory, anti-allergic, anti-microbial(antibacterial, antifungal, and antiviral) antioxidant, anti-cancer, and anti-diarrheal agents. Flavonoids are also reported to upregulate apoptotic activity in several cancers such as hepatic, pancreatic, breast, esophageal, and colon. Myricetin is a flavonol which is naturally present in fruits and vegetables and has shown possible nutraceutical value. Myricetin has been portrayed as a potent nutraceutical that may protect against cancer. The focus of the present review is to present an updated account of studies demonstrating the anticancer potential of myricetin and the molecular mechanisms involved therein. A better understanding of the molecular mechanism(s) underlying its anticancer activity would eventually help in its development as a novel anticancer nutraceutical having minimal side effects.

杨梅素调节Wnt/β-catenin信号通路对腰椎间盘突出症大鼠椎间盘退变的影响

目的:探究杨梅素(MYR)调节Wnt/β-连环蛋白(β-catenin)信号通路对腰椎间盘突出症(LDH)大鼠椎间盘退变的影响。方法:将大鼠随机分为Sham组、LDH组、MYR组、MYR+LiCl组(Wnt/β-catenin信号通路激活剂),每组12只,除Sham组外采用自体髓核移植法复制LDH大鼠模型,造模成功后进行药物干预,每天1次,持续28d。von Frey Hair纤维丝、辐射热痛觉测分析大鼠疼痛敏化行为;ELISA法检测血清肿瘤坏死因子(TNF-α)、白细胞介素1β(IL-1β)水平;HE染色法观察椎间盘组织病理变化;TUNEL染色法测定髓核细胞凋亡;免疫组化检测大鼠椎间盘组织中基质金属蛋白酶(MMP)13表达;Western blot分别检测Wnt/β-catenin信号通路蛋白表达。结果:与Sham组比较,LDH组大鼠髓核细胞皱缩、排列不规则,数量减少,纤维环破裂,MWT与TWL降低,TNF-α、IL-1β含量、椎间盘组织病理评分、髓核细胞凋亡率、MMP13、Wnt3a、β-catenin表达升高(P<0.05);与LDH组比较,MYR组髓核细胞形态、纤维环结构显著改善,大鼠MWT与TWL升高,TNF-α、IL-1β含量、椎间盘组织病理评分、髓核细胞凋亡率、MMP13、Wnt3a、β-catenin表达降低(P<0.05);Wnt/β-catenin信号通路激活剂LiCl可升高血清炎症因子水平,促进髓核细胞凋亡,加重椎间盘组织病理损伤,减弱了MYR对LDH大鼠椎间盘退变的延缓作用(P<0.05)。结论:MYR可能通过抑制Wnt/β-catenin信号通路的激活,降低炎症反应,减少髓核细胞凋亡,从而改善LDH大鼠的椎间盘退变。

杨梅素对α-淀粉酶的抑制机制研究

利用光谱学结合分子模拟和分子动力学技术,探究杨梅素对α-淀粉酶的抑制机理及其相互作用,阐释杨梅素抑制α-淀粉酶活性的分子机制。结果表明,杨梅素以混合型的方式抑制α-淀粉酶的活性,其半抑制浓度(IC_(50)值)为(9.25±0.31)mg/mL,抑制常数为(7.75±0.29)mg/mL。杨梅素主要通过氢键和范德华力与α-淀粉酶结合,结合常数K_(a)为10^(6)数量级。杨梅素能猝灭α-淀粉酶的荧光,猝灭方式为静态猝灭。当两者结合后,α-淀粉酶的二级结构由β-折叠向α-螺旋转变,使得酶的疏水性增加,结构变紧密。杨梅素能够进入α-淀粉酶的活性部位,与Leu162、Ala198、His201、Glu233、Ile235及Asp300等氨基酸残基发生相互作用。说明杨梅素与底物竞争酶的活性中心,阻碍酶催化底物,进而抑制α-淀粉酶的活性。

Myricetin protects against diet-induced obesity and ameliorates oxidative stress in C57BL/6 mice

Background： Mydcetin is a naturally occurring antioxidant commonly found in various plants. However, little information is available with respect to its direct anti-obesity effects. Objective： This study was undertaken to investigate the effect of myricetin on high-fat diet （HFD）-induced obesity in C57BL/6 mice. Results： Administration of myricetin dramatically reduced the body weight of diet-induced obese mice compared with solely HFD-induced mice. Several parameters related to obesity including serum glucose, triglyceride, and cholesterol were significantly de- creased in myricetin-treated mice. Moreover, obesity-associated oxidative stress （glutathione peroxidase （GPX） activity, total antioxidant capacity （T-AOC）, and malondialdehyde （MDA）） and inflammation （tumor necrosis factor-α （TNF-α）） were ameliorated in myricetin-treated mice. Further investigation revealed that the protective effect of my- ricetin against HFD-induced obesity in mice appeared to be partially mediated through the down-regulation of mRNA expression of adipogenic transcription factors peroxisome proliferator-activated receptor y （PPARF） and CCAAT/enhancer- binding protein a （C/EBPa）, and lipogenic transcription factor sterol regulatory element-binding protein lc （SREBP-1c）. Conclusions： Consumption of myricetin may help to prevent obesity and obesity-related metabolic complications.

The effects of pH, surfactant, ion concentration,coformer, and molecular arrangement on the solubility behavior of myricetin cocrystals

Pharmaceutical cocrystals are a promising technology that can be used to improve the solubility of poor aqueous compounds. The objective of this study was to systematically investigate the solubility of myricetin(MYR) cocrystals, including their kinetic solubility, thermodynamic solubility, and intrinsic dissolution rate(IDR). The effects of pH, surfactant, ion concentration, and coformers on the cocrystal solubility were evaluated. Furthermore, single crystal structures of MYR, myricetin–isonicotinamide(MYR–INM) and myricetin–caffeine(MYR–CAF) cocrystals were analyzed to discuss the possible reasons for the enhancement of cocrystal solubility from the perspective of the spatial structure.The results indicated that the kinetic solubility of MYR cocrystals was modulated by pH and cocrystal coformer(CCF) ionization in buffer solution, while it primarily depended on the CCF solubility in pure water. In addition, the solubility of MYR cocrystals was increased in a concentration dependent fashion by the surfactant or ion concentration. The thermodynamic solubility of MYR–INM(1:3) cocrystals decreased with the increases of the pH value of the dissolution media. The IDR of MYR cocrystals was faster than that of MYR in the same medium and extremely fast in pH 4.5 buffer. The improved solubility of MYR cocrystals was probably related to the alternate arrangements of MYR and INM/CAF molecules and increased intermolecular distance. The present study provides some references to investigate the solubility behavior of pharmaceutical cocrystals.

杨梅素通过调控NF-κB和炎症因子对肝脏缺血再灌注损伤的作用研究

目的观察杨梅素(Myr)对肝脏缺血再灌注损伤(HIRI)炎性因子的作用。方法将C57BL/6小鼠分为4组,手术组(Sham)、缺血再灌注组(HIRI)、低剂量杨梅素组(HIRI-Myr-L)和高剂量杨梅素组(HIRI-Myr-H),建立肝脏缺血再灌注损伤模型。测定谷丙转氨酶(ALT)和谷草转氨酶(AST);HE染色检测各组小鼠肝组织形态情况;Western blot和qRT-PCR检测各组肝组织中核转录因子-κB(NF-κB)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)的蛋白及mRNA表达情况。结果与HIRI组比较,HIRI-Myr-L、HIRI-Myr-H组ALT、AST水平均明显下降(P均<0.05);肝脏缺血面积明显减少,肝细胞肿胀变形减少;NF-κB、IL-6、TNF-α、IL-1β蛋白及mRNA表达水平降低(P均<0.05)。结论杨梅素能够抑制小鼠肝脏缺血再灌注诱导的NF-κB以及IL-6、TNF-α、IL-1β等炎症因子的表达升高,缓解肝脏损伤。

杨梅素对玉米淀粉消化的相互作用研究

为明确杨梅素对玉米淀粉在胃肠道的消化吸收过程中理化性质的影响,通过体外模拟玉米淀粉消化实验,发现杨梅素可以显著抑制玉米淀粉的消化,从而影响机体的血糖含量。加入杨梅素(1.7~15.3 mg/mL)可以将玉米淀粉的快速消化淀粉(RDS)含量从22.72%降至19.35%,抗性淀粉(RS)含量从18.11%提高至39.25%。通过静态流变学、差示扫描量热法(DSC)、X射线衍射法(XRD)、红外光谱法(FTIR)和扫描电镜(SEM)等实验,发现杨梅素是通过非共价作用与玉米淀粉结合,降低了玉米淀粉的热稳定性,破坏玉米淀粉原本的结晶结构,与淀粉形成更大的聚集体,使得淀粉的无定形区比例增加,影响淀粉的有序性,从而延缓玉米淀粉的消化吸收。该研究为杨梅素作为一种降血糖功能因子提供了理论依据。