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The pursuit of achieving both ceramic-like hardness and polymer-like flexibility in a coating, known as a polymer–ceramic hybrid coating, is a challenging yet highly desirable goal. The application of these coatings spans various domains such as foldable displays, wearable devices, maritime industries, and biomedical engineering. Particularly, endowing polymer–ceramic hybrid coatings with functions such as transparency, anti-liquid adhesion, anti-biofouling, and self-healing expand their potential in fields necessitating highly protective performance, which have gained significant attention in recent years. In this comprehensive review, our main objective is to provide interested readers with a clear framework for assessment and future exploration of this topic. We systematically outline the fundamentals of functional polymer-ceramic hybrid coatings, explaining their fabrication intricacies. Additionally, we explore their practical applications, intricately tailored to the unique requirements of each field. Concluding our review, we address the key challenges facing modern functional polymer–ceramic coatings and propose potential paths for future advancements. [Display omitted] [ABSTRACT FROM AUTHOR]

The occurrence of hyperlipidemia is significantly influenced by lipid synthesis, which is regulated by sterol regulatory element binding proteins (SREBPs), thus the development of drugs that inhibit lipid synthesis has become a popular treatment strategy for hyperlipidemia. Alisol B (ALB), a triterpenoid compound extracted from Alisma , has been reported to ameliorate no-nalcoholic steatohepatitis (NASH) and slow obesity. However, the effect of ALB on hyperlipidemia and mechanism are unclear. To examine the therapeutic impact of ALB on hyperlipidemia whether it inhibits SREBPs to reduce lipid synthesis. HepG2, HL7702 cells, and C57BL/6J mice were used to explore the effect of ALB on hyperlipidemia and the molecular mechanism in vivo and in vitro. Hyperlipidemia models were established using western diet (WD)-fed mice in vivo and oleic acid (OA)-induced hepatocytes in vitro. Western blot, real-time PCR and other biological methods verified that ALB regulated AMPK/mTOR/SREBPs to inhibit lipid synthesis. Cellular thermal shift assay (CETSA), molecular dynamics (MD), and ultrafiltration-LC/MS analysis were used to evaluate the binding of ALB to voltage-dependent anion channel protein-1 (VDAC1). ALB decreased TC, TG, LDL-c, and increased HDL-c in blood, thereby ameliorating liver damage. Gene set enrichment analysis (GSEA) indicated that ALB inhibited the biosynthesis of cholesterol and fatty acids. Consistently, ALB inhibited the protein expression of n-SREBPs and downstream genes. Mechanistically, the impact of ALB on SREBPs was dependent on the regulation of AMPK/mTOR, thereby impeding the transportation of SREBPs from endoplasmic reticulum (ER) to golgi apparatus (GA). Further investigations indicated that the activation of AMPK by ALB was independent on classical upstream CAMKK2 and LKB1. Instead, ALB resulted in a decrease in ATP levels and an increase in the ratios of ADP/ATP and AMP/ATP. CETSA, MD, and ultrafiltration-LC/MS analysis indicated that ALB interacted with VDAC1. Molecular docking revealed that ALB directly bound to VDAC1 by forming hydrogen bonds at the amino acid sites S196 and H184 in the ATP-binding region. Importantly, the thermal stabilization of ALB on VDAC1 was compromised when VDAC1 was mutated at S196 and H184, suggesting that these amino acids played a crucial role in the interaction. Our findings reveal that VDAC1 serves as the target of ALB, leading to the inhibition of lipid synthesis, presents potential target and candidate drugs for hyperlipidemia. [Display omitted] [ABSTRACT FROM AUTHOR]

Ice accretion may cause serious safety risk and huge economic loss for outdoor facilities. Herein, we report a waterborne polymeric coating based on a copolymer network of methacrylic acid (MAA), acrylamide (AM), N -2-hydroxyethyl acrylamide (HEAA), and methoxypolyethylene glycol (MPEG) with free polyethylene glycol (PEG) dispersed in it. Owing to the good compatibility of free PEG chains and the PEG side chains of the copolymer, the hydrogen bonding between acrylic copolymer and PEG, the free PEG chains can well be trapped in the network with some segments out of the mesh as short PEG chains are grafted on the coating surface, so that the surface has liquid-like properties. Water droplets can readily slip off on the coating surface with a small sliding angle (<30°). Particularly, the surface can hold the properties for a long duration upon water flushing, cycle of wetting-drying, and salt spraying tests. The polymer coating can find application in icing prevention and removal. [Display omitted] • A waterborne polymeric coating for antiicing and deicing can be fabricated based on a copolymer network with free polyethylene glycol chains dispersed in it. • The coating surface has liquid-like characters so that water droplets can readily slide it off. • The coating can prevent ice from accretion and is favorable for removing ice. • Upon water flushing, cycle of drying-wetting and salt spraying tests, the coating surface exhibits high durability. [ABSTRACT FROM AUTHOR]

• Hybrid superamphiphobic coating with repeatable adhesion and recyclability. • Snail-inspired versatile and industrially-viable strategy. • Hydrogel primer bonds fluorinated nanoparticles finish and substrates. • Reduce costs and minimize environmental footprint of superamphiphobic materials. • Crude-oil-anti-adhesion, temporary patterned and stretchable superamphiphobicity. Superamphiphobic surfaces with extreme repellency toward both water and oily liquids have been developed from various nanocomposites with fluorinated compounds. However, the inherent rigidity and low-surface-energy of these composites restrict their adhesion and practical application in adjusting the surface wettabilities of materials. Here we report a strategy to create hybrid superamphiphobic coating with rapid contact adhesion to various kinds of substrates, strong and controllable adhesive strength, unprecedented capability of mechanical deformations, facile removal, repeatable adhesion, and simple recyclization. Our approach, inspired by snail's ideal combination of hard shell and soft epiphragm, is versatile and industrially-viable because we use the hydrogel primer to bond the fluorinated nanoparticle finish and substrates. Considering the unique characteristics of these coatings as well as the wide range of available hydrogels and nanomaterials that can be used via this approach, we envision that this snail-inspired strategy will facilitate the development and large-scale production of superamphiphobic coatings. [ABSTRACT FROM AUTHOR]

• A tryptophan based hypercrosslinked polymer was prepared via facile one-step polymerization. • The polymer exhibited excellent adsorption selectivity and capacity for sulfonamides. • The polymer was used as sorbent for pipette tip solid phase extraction of sulfonamides. • The developed PT-SPE/HPLC method was validated in water, milk and meat samples. A novel tryptophan-based porous polymer is designed and synthesized via a facile one-step hypercrosslinking polymerization process, and applied as sorbent for extraction of trace sulfonamides in foodstuffs. The developed polymer has high surface area, large conjugate system, and abundant functional groups (e.g., π-π stacking, hydrogen bonding, hydrophobic and electrostatic attraction interactions), which endow it with superior affinity and high adsorption capacity for sulfonamides (16.16–59.29 mg g−1). The optimized SPE method is coupled with HPLC-DAD to create a sensitive and efficient protocol that provides good linearity (R2 ≥ 0.9979), low limits of detection, satisfactory recoveries (92.5–109.5 %) and high precisions (RSDs < 8.24). In addition, the newly proposed method greatly reduces the amount of adsorbent (2.0 mg) and organic solvent (2.0 mL) used. Adsorption kinetics, isotherms, and simulation calculations studies further reveal the presence of monolayer adsorption, chemical adsorption process, and multiple interactions. Thus, this work presents a polymer capable of multiple interactions for the pretreatment of trace sulfonamides in foodstuffs. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs), tetracyclines (TCs), and triphenylmethane dyes (TDs) are common organic pollutants, which may threat the human health or natural microbial communities. In this work, we report a novel multifunctional sorbent based on core-shell magnetic carboxylate-functionalized covalent organic frameworks composites (Fe 3 O 4 @COF–COOH) for the simultaneous adsorption of these target analytes via mixed-mode solid phase extraction. The behaviors of the synthetic composite for the adsorption of PAHs, TCs, and TDs were evaluated based on the Freundlich and Langmuir isotherm models. In combination with quantum chemistry calculations, it was found that the multiple interactions including π-π stacking, hydrogen bonding, and electrostatic attractions were existed between COF–COOH and guest molecules. The extraction parameters were optimized, and a novel simultaneous absorption-stepwise desorption (SASD) strategy for the enrichment of PAHs, TCs, and TDs was proposed. By coupling with HPLC-DAD method, the validation results revealed good linearities (R2 ≥ 0.9882) for all analytes. High sensitivity with LODs within the range of 0.003–0.008, 0.02–0.06, and 0.006–0.008 μg L−1 were obtained for PAHs, TCs, and TDs, respectively. High recoveries ranging from 93.6 to 105.8% were obtained with intra-day RSDs of 2.2–6.3% and inter-day RSDs of 3.2–6.5%. The obtained results demonstrated that the proposed SASD strategy using Fe 3 O 4 @COF–COOH as sorbents can be extended to other aqueous solutions consisting of trace multi-target analytes. A novel core-shell carboxylate-functionalized magnetic covalent organic frameworks composite was designed for the simultaneous adsorption of nonpolar PAHs, polar tetracyclines, and cationic triphenylmethane dyes via mixed-mode solid phase extraction. Image 1 • Carboxylate functionalized magnetic COFs were prepared through a facile strategy. • The resultant composites featured mixed-mode and multiple interactions. • It exhibited superior capture ability for PAHs, tetracyclines and cationic dyes. • The composites have good stability and can be easily recycled for reuse. • Quantum chemistry calculation was employed to study the adsorption mechanism. [ABSTRACT FROM AUTHOR]

Although ginsenoside Rb1 (G-Rb1) has exerted an inhibitory effect on renal fibrosis and progression of chronic kidney disease (CKD), its mechanism remains unknown. This study aims to explore the anti-fibrosis effect of G-Rb1 in unilateral ureter obstruction (UUO) mouse model and underlying mechanisms in HBSS-induced HK-2 cells. In vivo, renal function, kidney histological pathology, and autophagy-related protein molecules were assessed. Additionally, rapamycin, Deptor overexpression plasmid, Akt inhibitor, metformin, and a p38-MAPK inhibitor, as well as an ERK-MAPK inhibitor were used to evaluate the effect of AMPK/mTOR, Akt and MAPK signal pathways on the protective effect of G-Rb1 in HK-2 cells. Treatment with G-Rb1 significantly improved renal dysfunction. G-Rb1 reversed UUO-induced downregulation of p62, and upregulation of LC3 and the ratio of LC3 I/II, indicating that G-Rb1 restrained UUO-induced activation of autophagy. Furthermore, we found that treatment of HBSS-induced HK-2 cells with G-Rb1 resulted in AMPK/mTOR and ERK, p38 MAPKs signaling pathways regulated autophagy inhibition. These findings may explain, in part, the molecular mechanisms by which G-Rb1 could be applied in the treatment of patients with CKD, further suggesting that autophagy and its associated molecular signaling pathway may be new targets for the treatment of renal fibrosis and CKD. [ABSTRACT FROM AUTHOR]

Blockage of the urinary tract is often connected with renal function impediment, including reductions in glomerular filtration rate (GFR) and the power to control sodium as well as water elimination through urination. Melatonin, known to be the primary product of the pineal gland, prevents renal damage caused by ischemic reperfusion. However, the effects of melatonin on urinary obstruction, as well as release of obstruction induced kidney injury are still largely unknown. The aim of present study was to investigate the effect of melatonin on mediating protection against renal injury triggered from either bilateral ureteral obstruction (BUO) or BUO release (BUO-R). Adult male Sprague-Dawley rats (n = 60) were clustered into six treatment groups: sham treated-1; BUO-non-treated (24 h BUO only); BUO + melatonin; sham treated-2; BUO-48hR (24 h of BUO and then release for 2 days); and BUO-48hR + melatonin. Kidney tissues, blood and urine samples were obtained for further assessment. It was found that melatonin treatment remarkably promoted the recovery of the handling capacity of urinary excretion of water as well as sodium in BUO and BUO-48hR models. Melatonin treatment partially inhibited inflammatory cytokine expression and the downregulation of aquaporin (AQPs, AQP-1, -2 and -3) expression in these two models. Moreover, the cytoarchitecture of BUO rats exposed to melatonin was well preserved. Melatonin treatment potently prevents BUO or BUO-R induced renal injury, which may be partially attributed to restoring the expression of AQPs and inhibition of inflammatory response, as well as preserving renal ultrastructural integrity. [ABSTRACT FROM AUTHOR]

Shenmai injection (SMI), a traditional Chinese herbal medicine is widely used for the clinical treatment of cerebral infarction in China. Aim of the study: Tight junctions (TJs) are major components of the blood-brain barrier (BBB) that physically restrict the paracellular diffusion of blood-borne substances between endothelial cells into the CNS. TJ proteins are associated with cholesterol-enriched regions of plasma membrane known as lipid rafts, which are critical for the trafficking, positioning and function of TJ proteins. In this study, we investigated the effect of SMI on the expression and trafficking of the key TJ-associated protein, occludin, in lipid rafts. Using a neutral pH, rat cerebral microvessels were subjected to detergent-free density-gradient fractionation to isolate lipid rafts containing occludin. Transmission electron microscopy (TEM) was performed to study the effects of drug administration on ultrastructural changes to TJs. Western blotting (WB), immunofluorescence (IF), and co-immunoprecipitation (COIP) were used to observe the localization and function of TJ-associated proteins. We successfully isolated cerebral microvessels and separated lipid rafts from plasma membranes. With SMI treatment, extravasation of FITC-albumin decreased around the cerebral vessels by IF, the tight junctions were found to still be intact and the basement membrane appeared to be of uniform thickness in TEM. Compared with the untreated group, the co-expression of flotillin-1 and occludin in microvascular endothelial cells was increased and distributed continuously in SMI treatment as shown in double label IF. SMI significantly increased the translocation of occludin to lipid raft fractions by WB and COIP. SMI helps maintain the proper assembly of the TJ multiprotein complex in lipid rafts, thereby helping to preserve BBB functional integrity during focal cerebral ischemic insult. Our findings enhance our understanding of the mechanisms underlying the neuroprotective effect of SMI in cerebral ischemia. Image 1 [ABSTRACT FROM AUTHOR]

Histone lysine specific demethylase 1 (LSD1) is responsible for the demethylation of mono-/dimethylated lysine residue on histone proteins. LSD1 plays an extensive and essential role in the pathogenesis and progression of many human diseases such as cancers, and thus is becoming an attractive therapeutic target for cancer treatment. Tranylcypromine (TCP) is an important chemical template for developing irreversible LSD1 inhibitors, representing a major chemotype of clinical candidates. Here we report a novel pool of TCP derivatives with triazolopyrimidine as a privileged heterocylic motif. Starting from ticagrelor, a clinically available antiplatelet agent, as a hit compound, our medicinal efforts have led to the identification of compound 9j with nanomolar inhibitory potency against LSD1 as well as broad-spectrum antiproliferative activities against tumor cells. Enzyme studies show that compound 9j is selective over MAO-A/B enzymes, and also cellular active to elevate the expression of H3K4me2 by inhibiting LSD1 in cells. Furthermore, in a H1650 xenograft mouse model, oral administration of compound 9j at low 10 and 20 mg/kg dosages could enable a significant reduction in tumor size and a remarkable extension of survival. The current work is expected to provide an additional strategy to achieve new TCP-based LSD1 inhibitors. [Display omitted] • TCP-based triazolopyrimidine analogs were developed as novel LSD1 inhibitors. • Compound 9j had nanomolar potency against LSD1. • Compound 9j had good enzyme selectivity. • Compound 9j had robust in vivo antitumor activity. [ABSTRACT FROM AUTHOR]

The effect of static magnetic heat treatment on microstructures and mechanical properties of DZ483 alloy was investigated in combination with high temperature tensile experiments. It was found that the morphology of γ′ precipitates became spherical in the magnetic field of 12 T. Additionally, the application of magnetic field increased the tensile strength, elongation and micro-hardness of the superalloy. However, the magnetic field had no obvious effect on the reduction in area of alloys. The changes in microstructures could be attributed to the variation of the γ/γ′ lattice misfit and interfacial energy in the magnetic field. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is the second most common neurodegenerative disease, and no treatment is available to stop its progression. Studies have shown that the colonic pathology of PD precedes that of the brain. The 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model and the human A53T α-synuclein (α-syn) transgenic PD mouse model show colonic pathology and intestinal dopaminergic neuronal damage, which is comparable to the intestinal pathology of PD. Cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), which are brain-gut peptides, have neurotrophic and anti-inflammatory properties. Two GLP-1R agonists have already shown robust effects in phase II trials in PD patients. However, whether they have beneficial effects on colonic pathology in PD remains unclear. In this study, MPTP-treated mice and human A53T α-syn transgenic mice were intraperitoneally injected with a CCK analogue or Liraglutide, a GLP-1 analogue, once a day for 5 weeks. Levels of colonic epithelial tight junction proteins including occludin and zonula occludens-1 (ZO-1), inflammatory biomarkers including inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α), brain-derived neurotrophic factor (BDNF), tyrosine hydroxylase (TH) and α-syn were analyzed. The results show that the CCK analogue and Liraglutide both restored the disruption of intestinal tight junction, reduced colonic inflammation, inhibited colonic dopaminergic neurons reduction and the accumulation of α-syn oligomers in the colon of both PD mice models. This study suggested that CCK or GLP-1 analogues could be beneficial to the improvement of leaky gut barrier, inflammation, dopaminergic neuron impairment and accumulation of α-syn in the colon of PD patients. [ABSTRACT FROM AUTHOR]

Histone lysine-specific demethylase 1 (LSD1) is an important epigenetic modulator, and is implicated in malignant transformation and tumor pathogenesis in different ways. Therefore, the inhibition of LSD1 provides an attractive therapeutic target for cancer therapy. Based on drug repurposing strategy, we screened our in-house chemical library toward LSD1, and found that the EGFR inhibitor erlotinib, an FDA-approved drug for lung cancer, possessed low potency against LSD1 (IC 50 = 35.80 μM). Herein, we report our further medicinal chemistry effort to obtain a highly water-soluble erlotinib analog 5k (>100 mg/mL) with significantly enhanced inhibitory activity against LSD1 (IC 50 = 0.69 μM) as well as higher specificity. In MGC-803 cells, 5k suppressed the demethylation of LSD1, indicating its cellular activity against the enzyme. In addition, 5k had a remarkable capacity to inhibit colony formation, suppress migration and induce apoptosis of MGC803 cells. Furthermore, in MGC-803 xenograft mouse model, 5k treatment resulted in significant reduction in tumor size by 81.6% and 96.1% at dosages of 40 and 80 mg/kg/d, respectively. Our findings indicate that erlotinib-based analogs provide a novel structural set of LSD1 inhibitors with potential for further investigation, and may serve as novel candidates for the treatment of LSD1-overexpressing cancers. [Display omitted] • The quinazoline derivatives represent a new chemical class of LSD1 inhibitors. • Compound 5k had potent inhibitory activity against LSD1. • Compound 5k had good enzyme selectivity. • Compound 5k had robust in vivo antitumor activity. [ABSTRACT FROM AUTHOR]

A novel magnetic borate-modified MXene composite was prepared by in situ growth of Fe 3 O 4 particles onto the surface of phenylboronic acid modified Ti 3 C 2 T x nanosheets. The magnetic composite possesses highly selective recognition properties to catecholamines, and high adsorption capacity (up to 319.6 μmol g−1) for dopamine. Besides, the adsorption of urinary catecholamines can be accomplished within 2.0 min. The excellent adsorption performance can be assigned to its unique 2D layered structures, which helps to shorten the diffusion path and facilitate molecular transport. In addition, the multilayer adsorption and the synergetic interactions of borate affinity, van der Waals forces, hydrogen bonding and π-π stacking also contribute to the adsorption. By coupling the magnetic boronate affinity composites with high-performance liquid chromatography-fluorescence detection, a sensitive method for the determination of catecholamines in urine samples was proposed. The validation results revealed it can offer good linearities (correlation coefficients higher than 99%). The method detection limits were 0.06, 0.16, 0.03 and 0.14 ng mL−1 for norepinephrine, epinephrine, dopamine and isoprenaline, respectively, and relative recoveries for these catecholamines were in the range of 98.56–108.1%, 92.56–110.0%, 98.79–112.3% and 88.14–97.81%, respectively. The proposed method was successfully applied to analyze the catecholamines in the urine samples from 15 healthy volunteers and 16 patients with Alzheimer's disease. The results indicated that the magnetic borate-modified Mxene composite possesses superior extraction performance, and can be used as an outstanding candidate for the extraction of catecholamines in pre-clinical or clinical studies. [Display omitted] • Magnetic boronic acid modified Ti 3 C 2 T x composites were synthesized via hydrothermal method. • The combination of unique properties of Ti 3 C 2 T x nanosheets with magnetic separation property simplifies adsorption process. • The prepared sorbent exhibits excellent boronate affinity selectivity for catecholamines. • A sensitive analytical method for catecholamine neurotransmitters was established. [ABSTRACT FROM AUTHOR]

• Sulfonated functionalized magnetic COFs were prepared through a facile strategy. • The resultant composite featured mixed-mode and multiple interactions. • It exhibited excellent capture ability for β-agonists and fluoroquinolones. • Validated MSPE–LC–MS/MS method quantified β-agonists and fluoroquinolones in real samples. In this work, an efficient method for the determination of β-agonists and fluoroquinolones was established, based on a mixed-mode sorbent of magnetic sulfonated covalent organic framework composites. By coupling with HPLC–MS/MS, the main factors that affect the extraction procedure were optimized. Under the optimal conditions, the proposed HPLC–MS/MS method was successfully utilized for the extraction of β-agonists and fluoroquinolones in milk and pork meat samples. The method showed good linearities (R 2 ≥ 0.9916), and low LOQs of 0.1–0.2 ng g−1 for β-agonists and fluoroquinolones. The adsorption mechanism was investigated with the assistance of quantum chemistry calculation method, and it is worth noting that the sorbent relied mainly on the multiple adsorption mechanisms, including π–π stacking, hydrophobic, electrostatic attraction and hydrogen-bonding interactions. This work not only provides a simple method for the preparation of a mixed-mode sorbent, but also a routine analysis strategy for monitoring the illegal use of β-agonists and fluoroquinolones. [ABSTRACT FROM AUTHOR]

• DA is a dual-PPAR-α/γ and PPAR-γ partial agonist. • DA alleviates HFD-induced insulin resistance via PPAR-γ. • DA alleviates HFD-induced hepatic steatosis via PPAR-α. Dual-PPAR-α/γ agonist has the dual potentials to improve insulin resistance (IR) and hepatic steatosis associated with obesity. This study aimed to investigate whether dehydroabietic acid (DA), a naturally occurred compound, can bind to and activate both PPAR-γ and PPAR-α to ameliorate IR and hepatic steatosis in high-fat diet (HFD)-fed mice.. We found that DA formed stable hydrogen bonds with the ligand-binding domains of PPAR-γ and PPAR-α. DA treatment also promoted 3T3-L1 differentiation via PPAR-γ activation, and mitochondrial oxygen consumption in HL7702 cells via PPAR-α activation. In HFD-fed mice, DA treatment alleviated glucose intolerance and IR, and reduced hepatic steatosis, liver injury markers (ALT, AST), and lipid accumulation, and promoted mRNA expression of PPAR-γ and PPAR-α signaling elements involved in IR and lipid metabolism in vivo and in vitro , and inhibited mRNA expression of pro-inflammatory factors. Therefore, DA is a dual-PPAR-α/γ and PPAR-γ partial agonist, which can attenuate IR and hepatic steatosis induced by HFD-consumption in mice. [ABSTRACT FROM AUTHOR]

Caption: Proposed mechanism of the MG-mediated alleviation of AD. MG may be binding and activating PPAR-γ, then induce LXR , ABCA1 , and ApoE expression, which mediate the effective lysosomal clearance of Aβ in microglia. At the same time, MG inhibited the NF-κB and mRNA expression of inflammatory cytokines. In addition, it can activate Nrf2-ARE and reduce the production of ROS. • Magnolol is a natural PPAR-γ agonist with potent binding affinities. • Magnolol improves Aβ pathology in transgenic C. elegans via PPAR-γ. • Magnolol promoting microglia phagocytosis and the degradation of Aβ through activation of PPAR-γ. This study aims to investigate whether magnolol (MG), a natural neolignane compound, can prevent AD induced by beta-amyloid (Aβ) and the possible mechanisms involved. MG dose-dependently reduces Aβ deposition, toxicity and memory impairment caused by Aβ in transgenic C. elegans. More importantly, these effects are reversed by GW9662, a selective peroxisome proliferator-activated receptor-γ (PPAR-γ) antagonist. MG is more effective in enhancing PPAR-γ luciferase levels than honokiol (HK). Meanwhile, MG has the potential to bind with the ligand binding domain of PPAR-γ (PPAR-γ-LBD). As expected, MG inhibited the luciferase activity of NF-κB and its target genes of inflammatory cytokines, and this effect was blocked by GW9662. The luciferase activity of Nrf2-ARE expression can be activated by MG and decreased Aβ-induced reactive oxygen species (ROS). The target gene LXR of PPAR-γ is activated by MG, which upregulates ApoE and promotes microglia phagocytosis and the degradation of Aβ, and these effects were also reversed by GW9662. In summary, MG can attenuate Aβ-induced AD and the underlying mechanism is the reduction of inflammation and promotion of phagocytosis and degradation of Aβ, which is dependent on PPAR-γ. [ABSTRACT FROM AUTHOR]