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Abstract Butyrate (BU), a gut microbiota‐derived metabolite, has been reported to play a neuroprotective role in Parkinson's disease (PD). However, the specific molecular mechanism of BU has not been fully interpreted. This work aimed to verify the protective effects of BU against MPTP/MPP+‐induced neurotoxicity and explore the mechanisms involved. The results showed that BU protected against MPTP‐induced motor dysfunction and decreased tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels. Additionally, BU pretreatment improved PC12 cell viability and reduced MPP+‐induced PC12 cell apoptosis. BU treatment also attenuated MPP+‐stimulated oxidative stress and inflammatory response in PC12 cells. Furthermore, BU inhibited MPTP/MPP+‐induced hyperactivation of the JAK2/STAT3 signaling in mice and PC12 cells. Besides, a JAK2 agonist, Coumermycin A1 (C‐A1), substantially reversed BU‐mediated inhibition on JAK2/STAT3 phosphorylation in MPP+‐challenged PC12 cells and abated BU‐induced repression on MPP+‐triggered apoptosis, oxidative stress, and inflammatory response in PC12 cells. To sum up, BU might exert neuroprotective effects against MPP+/MPTP‐induced neurotoxicity by inactivating the JAK2/STAT3 signaling.

AIM: To investigate the effect of repeated intravitreal injection of ranibizumab and aflibercept on corneal nerve of patients with macular edema.METHODS: A total of 64 patients(64 eyes)enrolled in our hospital from June 2021 to June 2022 were treated with intravitreal injection of anti-vascular endothelial growth factor(VEGF). There were 20 cases(20 eyes)of diabetic macular edema, 19 cases(19 eyes)of wet age-related macular degeneration and 25 cases(25 eyes)of retinal vein occlusion. Corneal confocal microscope was used to collect images of corneal subbasal nerve plexus before injections and at 1mo after each intravitreal injection based on 3+pro re nata(PRN)treatment regimen. Furthermore, the length and density of corneal nerve were measured.RESULTS: There was no significant difference in corneal nerve density of patients injected with aflibercept between pre-injection and post-injection(P>0.05), while the corneal nerve length after 2nd and 3rd injections was lower than that of pre-injection(all P0.05), and there was no significant differences in corneal nerve density and length after 3 injections of the two drugs(all P>0.05).CONCLUSION: Repeated intravitreal anti-VEGF drug may affect corneal nerve to some extent. For patients who need repeated intravitreal injections of anti-VEGF, attention should be paid to the changes of corneal nerves.

AIM: To evaluate the expression of systemic immune-inflammation index(SII),neutrophil/lymphocyte ratio(NLR)and platelet/lymphocyte ratio(PLR)and their value in patients with retinal vein occlusion(RVO).METHODS: A total of 57 patients with CRVO,88 patients with BRVO and 89 normal subjects were recruited in Dalian No.3 People's Hospital from August 2019 to August 2021. Blood cell counts and SII,NLR,and PLR levels were compared. Receiver operating characteristic(ROC)curve was used to determine the predictive value of SII in the occurrence of RVO.RESULTS:Neutrophil,white blood cell counts, NLR and SII were higher in the CRVO and BRVO groups than in the control group, and there was a significant difference(all P

ObjectiveArteriolosclerosis cerebral small vessel disease (CSVD) is a common type of CSVD. This study aimed to explore the factors associated with cognitive function and total MRI burden related to the disease.MethodsThe demographic characteristics, clinical manifestations, cognitive function score, Barthel Index (BI), blood test index, and follow-up results of arteriolosclerosis CSVD patients treated for the first time in our hospital from January 2014 to August 2022 were collected. White matter hyperintensity (WMH) Fazekas score, total MRI burden, and cerebral atrophy grade were evaluated according to brain MRI findings. Factors associated with CSVD cognitive function were analyzed by binary logistic regression. The correlative factors related to the total MRI burden of CSVD were analyzed by ordered multiple logistic regression.ResultsA total of 146 patients were included in this study, of which 132 cases (90.4%) had hypertension. There were 108 patients (74.0%) with cognitive dysfunction, 97 patients (66.4%) with balance and gait disorders, and 83 patients (56.8%) with moderate-to-severe dependence in daily life (BI ≤ 60 points). Of 146 patients, 79 (54.1%) completed clinical and imaging follow-ups for a median of 3 years. The number of patients with cognitive impairment and BI ≤ 60 points after follow-up significantly increased compared with the first admission (P < 0.001). There were also significant differences in total MRI burden (P = 0.001), WMH Fazekas score, and cerebral atrophy grade (P < 0.001). Mean age (P = 0.012), median deep WMH Fazekas score (P = 0.028), and median deep (P < 0.001) and superficial (P =0.002) cerebral atrophy grade of patients with cognitive impairment at first admission were all higher than those with non-cognitive impairment. Multivariate analysis showed that deep cerebral atrophy was independently and significantly associated with cognitive impairment of CSVD (P = 0.024), and hypertension was significantly and independently associated with total MRI burden (P = 0.001).ConclusionThe disease course of arteriolosclerosis CSVD may be related to cognitive function and total MRI burden. Deep cerebral atrophy was an independent risk factor for cognitive dysfunction in arteriolosclerosis CSVD, and hypertension was an independent risk factor for total MRI burden.

Abstract Background FMRP is a selective mRNA-binding protein that regulates protein synthesis at synapses, and its loss may lead to the impairment of trace fear memory. Previously, we found that FMRP levels in the hippocampus of rats with post-traumatic stress disorder (PTSD) were decreased. However, the mechanism underlying these changes remains unclear. Methods Forty-eight male Sprague-Dawley rats were randomly divided into four groups. The experimental groups were treated with the single-prolonged stress (SPS) procedure and injected with a lentivirus-mediated inhibitor of miR-142-5p. Behavior test as well as morphology and molecular biology experiments were performed to detect the effect of miR-142 downregulation on PTSD, which was further verified by in vitro experiments. Results We found that silence of miRNA-142 (miR-142), an upstream regulator of FMRP, could alleviate PTSD-like behaviors of rats exposed to the SPS paradigm. MiR-142 silence not only decreased the levels of proinflammatory mediators, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α, but also increased the expressive levels of synaptic proteins including PSD95 and synapsin I in the hippocampus, which was one of the key brain regions associated with PTSD. We further detected that miR-142 silence also downregulated the transportation of nuclear factor kappa-B (NF-κB) into the nuclei of neurons and might further affect the morphology of neurons. Conclusions The results revealed miR-142 downregulation could alleviate PTSD-like behaviors through attenuating neuroinflammation in the hippocampus of SPS rats by binding to FMRP.

AIM: To investigate the clinical effectiveness of conbercept intravitreal injection combined with panretinal photocoagulation for ischemic central retinal vein occlusion.METHODS: A retrospective study has been conducted on 80 patients(80 eyes)of ischemic central retinal vein occlusion diagnosed and treated at Dalian No.3 People's Hospital from January 2017 to January 2019. These 80 patients have been divided into two groups based on treatment methods. In Group A, 40 patients(40 eyes)were given 3+PRN intravitreal injection of conbercept combined with panretinal photocoagulation. In Group B, 40 patients(40 eyes)accepted the treatment of 3+PRN intravitreal injection with conbercept. The best corrected visual acuity(BCVA)and central macular thickness(CMT)before and after treatment were recorded respectively at 3mo, 6mo and 12mo, and the clinical effectiveness and adverse reactions were observed and documented.RESULTS: After 12mo: In group A, BCVA improved from 1.05±0.58 to 0.41±0.37(P0.05). In group A, CMT changed from 592.30±79.75μm to 260.08±86.23μm(P

Abstract. Background:. The detection of polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes (POEMS) syndrome at early stage is challenging for neurologists. Since polyneuropathy could be the first manifestation, it could be misdiagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP). The present study aimed to determine the clinical and electrophysiological features of POEMS syndrome to distinguish from CIDP. Methods:. The data of a group of patients with POEMS (n = 17) and patients with CIDP (n = 17) in Zhongshan Hospital Fudan University from January 2015 to September 2017 were analyzed in this retrospective study. The clinical features, neurological symptoms, and electrophysiological findings were compared between the two groups. Results:. Clinically, patients with POEMS demonstrated significantly more neuropathic pain in the lower extremities than patients with CIDP (58.8% vs. 11.8%, P = 0.01). Multisystem features like edema, skin change, organomegaly, and thrombocytosis were also pointed towards the diagnosis of POEMS syndrome. Electrophysiologically, terminal latency index (TLI) was significantly higher in patients with POEMS than that in patients with CIDP (median nerve: 0.39 [0.17–0.52] vs. 0.30 (0.07–0.69), Z = –2.413, P = 0.016; ulnar nerve: 0.55 [0.23–0.78] vs. 0.42 [0.12–0.70], Z = –2.034, P = 0.042). Patients with POEMS demonstrated a higher frequency of absent compound muscle action potential of the tibial nerve (52.9% vs. 17.6%, P = 0.031), less conduction block (ulnar nerve: 0 vs. 35.3%, P = 0.018), and less temporal dispersion (median nerve: 17.6% vs. 58.8%, P = 0.032) than CIDP group. The combination of positive serum monoclonal protein and high TLI (if either one or both were present) discriminated POEMS from CIDP with a sensitivity of 94.1% and 47.1% and specificity of 76.5% and 100.0%, respectively. Conclusions:. POEMS syndrome could be distinguished from CIDP through typical clinical and electrophysiological characteristics in practice. The combination of serum monoclonal protein and high TLI might raise the sensitivity of detecting POEMS syndrome.

Abstract Background Pistachio (Pistacia vera), one of the most important commercial nut crops worldwide, is highly adaptable to abiotic stresses and is tolerant to drought and salt stresses. Results Here, we provide a draft de novo genome of pistachio as well as large-scale genome resequencing. Comparative genomic analyses reveal stress adaptation of pistachio is likely attributable to the expanded cytochrome P450 and chitinase gene families. Particularly, a comparative transcriptomic analysis shows that the jasmonic acid (JA) biosynthetic pathway plays an important role in salt tolerance in pistachio. Moreover, we resequence 93 cultivars and 14 wild P. vera genomes and 35 closely related wild Pistacia genomes, to provide insights into population structure, genetic diversity, and domestication. We find that frequent genetic admixture occurred among the different wild Pistacia species. Comparative population genomic analyses reveal that pistachio was domesticated about 8000 years ago and suggest that key genes for domestication related to tree and seed size experienced artificial selection. Conclusions Our study provides insight into genetic underpinning of local adaptation and domestication of pistachio. The Pistacia genome sequences should facilitate future studies to understand the genetic basis of agronomically and environmentally related traits of desert crops.

Post-traumatic stress disorder (PTSD) is usually accompanied by anxiety symptoms and decreased expression of brain-derived neurotrophic factor (BDNF), which played an important role in promoting neuronal proliferation and survival. Methyl CpG-binding protein 2 (MeCP2) is a positive mediator of BDNF and is regulated by miR-132-3p. In the present study, we explored the possible molecular mechanism of miR-132, focusing on the involvement of MeCP2 and BDNF in the formation of anxiety-like symptoms of PTSD. Single prolonged stress (SPS) was used to establish a model of PTSD in adult rats and the anxiety-like behavior was tested by the elevated plus-maze (EPM). The level of miR-132 in the prefrontal cortex (PFC) was increased and intraventricular injection of anti-miR-132 could significantly improve the anxiety-like behavior of rats exposed to SPS through MeCP2 and the subsequent upregulation of BDNF levels. Then tropomyosin-related kinase B (TrkB) and downstream signals, including MAP kinase ERK1/2 and phosphoinositol 3-kinase (PI3K)/Akt pathways, were activated by BDNF upregulation, and might participate in regulating dendritic complexity and the expression of postsynaptic density-95 (PSD95) and synapsin I in the PFC of SPS rats. Furthermore, we found that the apoptosis of cells in PFC induced by SPS procedure could be alleviated by miR-132 inhibition. Our results suggest that miR-132 might be involved in the formation of anxiety-like symptoms of adult rat PTSD models by targeting MeCP2, and this effect is related to BDNF/TrkB and its downstream ERK and Akt signaling pathways.

AIM: To observe the attenuation of ethanol extract of Herba Scutellaria barbata (SE) against diabetic retinopathy (DR) and its engaged mechanism. METHODS: C57BL/6J mice were intraperitoneally injected with streptozotocin (STZ, 55 mg/kg) for 5 consecutive days to induce diabetes. The diabetic mice were orally given with SE (100, 200 mg/kg) for 1mo at 1mo after STZ injection. Blood-retinal barrier (BRB) breakdown was detected by using Evans blue permeation assay. Real-time polymerase chain reaction (RT-PCR), Western blot and immunofluorescence staining were used to detect mRNA and protein expression. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum contents of tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β. RESULTS: SE (100, 200 mg/kg) reversed the breakdown of BRB in STZ-induced diabetic mice. The decreased expression of retinal claudin-1 and claudin-19, which are both tight junction (TJ) proteins, was reversed by SE. SE decreased the increased serum contents and retinal mRNA expression of TNF-α and IL-1β. SE also decreased the increased retinal expression of intercellular cell adhesion molecule-1 (ICAM-1). SE reduced the increased phosphorylation of nuclear factor kappa B (NFκB) p65 and its subsequent nuclear translocation in retinas from STZ-induced diabetic mice. Results of Western blot and retinal immunofluorescence staining of ionized calcium-binding adapter molecule 1 (Iba1) demonstrated that SE abrogated the activation of microglia cells in STZ-induced diabetic mice. CONCLUSION: SE attenuates the development of DR by inhibiting retinal inflammation and restoring the decreased expression of TJ proteins including claudin-1 and claudin-19.

Cognitive impairment in Alzheimer’s disease (AD) is usually accompanied by synaptic loss in both the hippocampus and neocortex. In the early stage of AD, amyloid β-induced synapse changes is the main reason, while in the later stage, the accumulation of Tau protein promotes synapse degeneration as the key factor leading to dementia. MicroRNA (miRNA) is closely related to the expression changes of many AD-related genes. One of the most abundant brain-enriched miRNAs is miR-132, which has been shown to regulate both neuron morphogenesis and plasticity. It has been reported that miR-132 is significantly reduced in the brains of Alzheimer’s patients. Genetic deletion of miR-132 in mice promotes Aβ deposition, leading to impaired memory and enhanced Tau pathology, but how the miRNA-mediated gene expression dysregulation contributes to AD pathology remains unclear. Here we found the possible downstream target of miR-132 by in silico analysis, namely C1q. C1q is the primary protein of classical complement cascade, which is highly expressed in the synaptic regions of the central nervous system in Alzheimer’s patients. However, it is not clear whether miR-132 plays a role in AD through regulating C1q. To address this question, the APP/PS1 transgenic mice were transfected with miR-132 and given C1 inhibitors. Behavior tests were conducted to assess memory and cognitive abilities seven days after administration. In addition, we analyzed the expression of PSD95, Synapsin-1 and phosphorylated (p)-Synapsin. We found that the expression levels of the synaptic proteins treated with miR-132 or C1INH were significantly increased compared with the AD group. Further RT-qPCR result suggested that miR-132 might regulate C1q expression in AD.

AIM:To establish the rat model of streptozotocin (STZ)-induced diabetic retinopathy (DR), which is the most common cause of visual loss and blindness in patients with diabetes, and observe the gene expression of vascular endothelial growth factor (VEGF) and its receptors during the development of DR.METHODS:A rat model of diabetes was established by intraperitoneal injection of STZ. The diabetic rats were housed for 2, 3 and 4 months after the development of diabetes. Retinal histopathological observation was performed. The retinal vessels were observed by immunofluorescence staining by CD31. The mRNA expression of VEGF, VEGF receptor 1 and 2 (VEGFR1/2) in rat retina was detected by reverse transcription-polymerase chain reaction (RT-PCR) analysis.RESULTS:Retinal histopathological observation showed the morphological changes of inner nuclear layer (INL) and outer nuclear layer (ONL) at any time-point, and also demonstrated the increased new vessels at both 3, 4 months after the development of diabetes. The CD31 staining results showed that the number of vessels was increased in the retinas of diabetic rats at both 3 and 4 months after the development of diabetes. As compared to the normal rats, the mRNA expression of VEGF was increased in retinas of diabetic rats at 3 months after the development of diabetes, while VEGFR1 and VEGFR2 mRNA expression was increased at 2, 3 and 4 months after the development of diabetes.CONCLUSION: Taken together, our results demonstrated that DR was occurred at 3 months after the development of diabetes, and the mRNA expression of VEGF, VEGFR1 and VEGFR2 were increased in the process of DR. The present study further evidenced the involvement of VEGF and its receptors in the process of DR.

In the title compound, [Zn(C12H9O2)2(C12H12N2)]·0.5H2O, the water molecule lies on a twofold rotation axis. The ZnII atom is coordinated by three O atoms from two 1-naphthylacetate ligands, one monodentate and the other asymmetric bidentate chelate, and two N atoms from a 5,5′-dimethyl-2,2′-bipyridine ligand, giving an irregular environment. In the crystal, the complex molecules are interlinked through the water molecule by O—H...Ocarboxylate hydrogen bonds, together with weak C—H...O and bipyridine ring π–π stacking interactions [ring centroid separation = 3.761 (2) Å], giving a two-dimensional network structure.

In the title compound, [Co(C8H5Cl2O3)(C12H12N2)], the CoII atom, lying on a twofold rotation axis, is coordinated by four O atoms from two chelating 2,4-dichlorophenoxyacetate ligands and two N atoms from a 5,5′-dimethyl-2,2′-bipyridine ligand, displaying a distorted octahedral geometry. A three-dimensional supramolecular structure is formed through intermolecular C—H...O hydrogen bonds and π–π stacking interactions between the pyridine and benzene rings [centroid–centroid distance = 3.779 (2) Å].

In the title complex, [Co(C8H9N2O4)2(H2O)2]·2C3H7NO, the CoII cation (site symmetry overline1) is six-coordinated by two 5-carboxy-2-propyl-1H-imidazole-4-carboxylate ligands and two water molecules in a distorted octahedral environment. In the crystal structure, the complex molecules and dimethylformamide solvent molecules are linked by extensive O—H...O and N—H...O hydrogen bonding into sheets lying parallel to (21overline{1}).

In the title compound, [Cd(C8H7O2)2(C3H4N2)2(H2O)], the CdII atom is coordinated by four carboxylate O atoms from two bidentate chelating 4-methylbenzoate ligands, two N atoms from two imidazole ligands and one water molecule in a distorted pentagonal bipyramidal geometry. Intermolecular O—H...O hydrogen bonds between the coordinated water molecule and the carboxylate O atoms of 4-methylbenzoate lead to an infinite chain. These chains are further self-assembled into a two-dimensional layer through N—H...O hydrogen bonds between the imidazole ligands and carboxylate groups. One of the imidazole ligands is disordered over two positions with site-occupancy factors of 0.737 (4) and 0.263 (4).

In the mononuclear title compound, [Cd(C12H9O2)2(C3H4N2)2], the CdII centre has a distorted octahedral coordination geometry defined by four O atoms from two naphthaleneacetate ligands and two N atoms from two imidazole ligands. The molecules are linked by N—H...O hydrogen bonds, forming a layer network.

A new coordination polymer, [Cu(C7H2N2O7)(C5H5NO)]n, exhibits a double-chain structure, in which 3,5-dinitro-2-oxidobenzoate and 3-hydroxypyridine both act as bridging ligands, connecting adjacent copper(II) centers to form an infinite double-stranded chain. The asymmetric unit contains one CuII ion, one 3,5-dinitro-2-oxidobenzoate ligand and a 3-hydroxypyridine ligand. Coordination by one N atom and three O atoms from two different 3,5-dinitro-2-oxidobenzoate ligands and a 3-hydroxypyridine ligand creates a square-planar CuII center, which is augmented by a less tightly bonded fifth phenol O atom to form a square-pyramidal five-coordinate complex with an essentially planar base. The double-stranded chains are stabilized by intrachain π–π interactions [the centroid-to-centroid distance between adjacent aromatic rings is 3.719 (7) Å], and further linked through O—H...O hydrogen bonds, forming a three-dimensional supramolecular network.

In the title complex, [Ni(C3H4N2)6](C6H5O2S)2, the NiII atom displays an octahedral coordination geometry, defined by six N atoms from the imidazole ligands. Intermolecular N—H...O hydrogen-bonding interactions between the cationic complex and 3-thienylacetate anions form a three-dimensional network architecture. The two 3-thienylacetate anions are disordered, with occupancy ratios of circa 0.774 (1):0.226 (1) and ca 0.753 (5):0.247 (5).

In the title three-dimensional coordination polymer, {[Fe(C8H5NO4)(H2O)]·2H2O}n, the FeII atom exhibits a distorted octahedral geometry, being coordinated by one N and four O atoms from four 5-aminoisophthalate ligands and one water molecule. In addition, the crystal structure is stabilized by numerous O—H...O and N—H...O hydrogen bonds.

In the title mononuclear complex, [Ni(C8H7O2)2(C5H5N)2(H2O)], the NiII atom is in a distorted octahedral arrangement, coordinated by three carboxylate O atoms from one bidentate 4-methylbenzoate ligand and one monodentate 4-methylbenzoate ligand, two N atoms from pyridine ligands, axially positioned, and a water molecule. The equatorially positioned water molecule and uncoordinated carboxylate O atom form an intramolecular hydrogen bond. An intermolecular O—H...O hydrogen bond between the coordinated water molecule and carboxylate O atom of the 4-methylbenzoate ligand forms infinite chains along the b axis. These chains are connected by C—H...π interactions.

In the title mononuclear complex, [Zn(C11H7O3)2(H2O)4], the ZnII atom is located on a centre of inversion and is coordinated by two O atoms from two 1-hydroxy-2-naphthoate ligands and four water molecules in an octahedral geometry. The structure is consolidated by intermolecular O—H...O hydrogen bonding, as well as by a π–π stacking interaction [centroid–centroid distance 3.762 (2)Å] between adjacent naphthyl ring systems.

A simple one-equilibrium memristor-based chaotic system (MCS) is established by combining a non-ideal memristor with a three-dimensional (3D) chaotic system with six polynomial terms. Its dynamical characteristics are studied and verified by some simulation experiments. The proposed MCS produces chaos via period-doubling bifurcation and maintains steady and robust chaotic behaviors unaffected by initial conditions. By changing the parameter values, the oscillation amplitudes of all the variables will be enlarged or shrunk on a large scale, indicating the existence of large-scale chaotic amplitude modulation. The finite-time synchronization (FTS) of the proposed MCS is studied, and the sufficient conditions of FTS based on simple feedback control are established via strict theoretical analysis. Numerical simulations demonstrate the correctness of the obtained results. [ABSTRACT FROM AUTHOR]

It is well established that mitochondria play a critical role in the metabolic and physiological adaptation of skeletal muscle to enhanced contractile activity. Several redox-sensitive signaling pathways such as PGC-1α, AMPK, IGF/Akt/mTOR, SIRT, NFκB, and FoxO are involved with extensive crosstalk to regulate vital cellular functions such as mitochondrial biogenesis, mitochondrial fusion and fission dynamics, autophagy/mitophagy, and apoptosis under altered demand and stress. However, when muscles cease contraction, such as during immobilization and denervation, mitochondria undergo a series of detrimental changes characterized by downregulation of PGC-1α and antioxidant defense, increased ROS generation, activated FoxO, NFκB, and inflammation, enhanced ubiquitination, and finally mitophagy and apoptotic cascades. The phenotypic outcome of the discord of mitochondrial homeostasis is elevated proteolysis and muscle atrophy. The demonstration that PGC-1α overexpression via transgene or in vivo DNA transfection can restore mitochondrial homeostasis and reverse myocyte atrophy supports the “mitostasis theory of muscle atrophy”.

Abstract Background Metabolic dysfunction-associated fatty liver disease (MAFLD) is a typical hepatic steatosis with metabolic dysfunction. The composite dietary antioxidant index (CDAI) measures individual antioxidant capacity, and the relationship with MAFLD has received little attention. Our goal is to explore the association of CDAI with MAFLD. Methods Participants were selected from the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2020. CDAI was calculated basing on six dietary antioxidants, including zinc, selenium, carotenoids, and vitamins A, C, and E. Univariate regression and multivariable logistic regression analysis were conducted to evaluate the correlation between CDAI and MAFLD. We performed subgroup analysis to study the correlation in various populations. Results A total of 18,163 participants, including 13,969 MAFLD and 4,194 non-MAFLD, were included. CDAI was significantly negatively correlated with MAFLD. After adjusting for all confounders (including age, gender, race, marital status, poverty ratio, education level, drinking status, smoking status, and physical activity), individuals in the highest quartile of CDAI exhibited a 27% lower likelihood of developing MAFLD than those in the lowest quartile (OR = 0.73; 95% CI [0.66, 0.81], p

PRKAG2 is required for the maintenance of cellular energy balance. PRKAG2-AS1, a long non-coding RNA (lncRNA), was found within the promoter region of PRKAG2. Despite the extensive expression of PRKAG2-AS1 in endothelial cells, the precise function and mechanism of this gene in endothelial cells have yet to be elucidated. The localization of PRKAG2-AS1 was predominantly observed in the nucleus, as revealed using nuclear and cytoplasmic fractionation and fluorescence in situ hybridization. The manipulation of PRKAG2-AS1 by knockdown and overexpression within the nucleus significantly altered PRKAG2 expression in a cis-regulatory manner. The expression of PRKAG2-AS1 and its target genes, PRKAG2b and PRKAG2d, was down-regulated in endothelial cells subjected to oxLDL and Hcy-induced injury. This finding suggests that PRKAG2-AS1 may be involved in the mechanism behind endothelial injury. The suppression of PRKAG2-AS1 specifically in the nucleus led to an upregulation of inflammatory molecules such as cytokines, adhesion molecules, and chemokines in endothelial cells. Additionally, this nuclear suppression of PRKAG2-AS1 facilitated the adherence of THP1 cells to endothelial cells. We confirmed the role of nuclear knockdown PRKAG2-AS1 in the induction of apoptosis and inhibition of cell proliferation, migration, and lumen formation through flow cytometry, TUNEL test, CCK8 assay, and cell scratching. Finally, it was determined that PRKAG2-AS1 exerts direct control over the transcription of PRKAG2 by its binding to their promoters. In conclusion, downregulation of PRKAG2-AS1 suppressed the proliferation and migration, promoted inflammation and apoptosis of endothelial cells, and thus contributed to the development of atherosclerosis resulting from endothelial cell injury.