Mouse serum albumin induces neuronal apoptosis and tauopathies.

The elderly frequently present impaired blood-brain barrier which is closely associated with various neurodegenerative diseases. However, how the albumin, the most abundant protein in the plasma, leaking through the disrupted BBB, contributes to the neuropathology remains poorly understood. We here demonstrated that mouse serum albumin-activated microglia induced astrocytes to A1 phenotype to remarkably increase levels of Elovl1, an astrocytic synthase for very long-chain saturated fatty acids, significantly promoting VLSFAs secretion and causing neuronal lippoapoptosis through endoplasmic reticulum stress response pathway. Moreover, MSA-activated microglia triggered remarkable tau phosphorylation at multiple sites through NLRP3 inflammasome pathway. Intracerebroventricular injection of MSA into the brains of C57BL/6J mice to a similar concentration as in patient brains induced neuronal apoptosis, neuroinflammation, increased tau phosphorylation, and decreased the spatial learning and memory abilities, while Elovl1 knockdown significantly prevented the deleterious effect of MSA. Overall, our study here revealed that MSA induced tau phosphorylation and neuron apoptosis based on MSA-activated microglia and astrocytes, respectively, showing the critical roles of MSA in initiating the occurrence of tauopathies and cognitive decline, and providing potential therapeutic targets for MSA-induced neuropathology in multiple neurodegenerative disorders.

Thrombomodulin reduces α-synuclein generation and ameliorates neuropathology in a mouse model of Parkinson's disease.

The neurotoxic α-synuclein (α-syn) oligomers play an important role in the occurrence and development of Parkinson's disease (PD), but the factors affecting α-syn generation and neurotoxicity remain unclear. We here first found that thrombomodulin (TM) significantly decreased in the plasma of PD patients and brains of A53T α-syn mice, and the increased TM in primary neurons reduced α-syn generation by inhibiting transcription factor p-c-jun production through Erk1/2 signaling pathway. Moreover, TM decreased α-syn neurotoxicity by reducing the levels of oxidative stress and inhibiting PAR1-p53-Bax signaling pathway. In contrast, TM downregulation increased the expression and neurotoxicity of α-syn in primary neurons. When TM plasmids were specifically delivered to neurons in the brains of A53T α-syn mice by adeno-associated virus (AAV), TM significantly reduced α-syn expression and deposition, and ameliorated the neuronal apoptosis, oxidative stress, gliosis and motor deficits in the mouse models, whereas TM knockdown exacerbated these neuropathology and motor dysfunction. Our present findings demonstrate that TM plays a neuroprotective role in PD pathology and symptoms, and it could be a novel therapeutic target in efforts to combat PD. Schematic representation of signaling pathways of TM involved in the expression and neurotoxicity of α-syn. A TM decreased RAGE, and resulting in the lowered production of p-Erk1/2 and p-c-Jun, and finally reduce α-syn generation. α-syn oligomers which formed from monomers increase the expression of p-p38, p53, C-caspase9, C-caspase3 and Bax, decrease the level of Bcl-2, cause mitochondrial damage and lead to oxidative stress, thus inducing neuronal apoptosis. TM can reduce intracellular oxidative stress and inhibit p53-Bax signaling by activating APC and PAR-1. B The binding of α-syn oligomers to TLR4 may induce the expression of IL-1ß, which is subsequently secreted into the extracellular space. This secreted IL-1ß then binds to its receptor, prompting p65 to translocate from the cytoplasm into the nucleus. This translocation downregulates the expression of KLF2, ultimately leading to the suppression of TM expression. By Figdraw.

[Prediction and analysis of Q-markers of Elephantopus scaber based on its UPLC fingerprint, content determination of components, and in vitro a nti-tumor activity].

This study aimed to provide scientific evidence for predicting quality markers(Q-markers) of Elephantopus scaber by establishing UPLC fingerprint of E. scaber from different geographical origins and determining the content of 13 major components, as well as conducting in vitro anti-cancer activity investigation of the main components. The chromatographic column used was Waters CORTECS UPLC C_(18)(2.1 mm×150 mm, 1.6 µm), and the mobile phase consisted of acetonitrile and 0.1% formic acid solution(gradient elution). The column temperature was set at 30 ℃, and the flow rate was 0.2 mL·min~(-1). The injection volume was 1 µL, and the detection wavelength was 240 nm. The UPLC fingerprint of E. scaber was fitted using the Similarity Evaluation System for Chromatographic Fingerprint of Traditional Chinese Medicine(2012 edition) to determine common peaks, evaluate similarity, identify and determine the content of major components. The CCK-8 assay was used to explore the inhibitory effect of the main components on the proliferation of lung cancer cells. The results showed that in the established UPLC fingerprint of E. scaber, 35 common peaks were identified. Thirteen major components, including neochlorogenic acid(peak 1), chlorogenic acid(peak 2), cryptochlorogenic acid(peak 3), caffeic acid(peak 4), schaftoside(peak 6), galuteolin(peak 9), isochlorogenic acid B(peak 10), isochlorogenic acid A(peak 12), isochlorogenic acid C(peak 18), deoxyelephantopin(peak 28), isodeoxyelephantopin(peak 29), isoscabertopin(peak 31), and scabertopin(peak 32) were identified and quantified, and a quantitative analysis method was established. The results of the in vitro anti-cancer activity study showed that deoxyelephantopin, isodeoxyelephantopin, isoscabertopin, and scabertopin in E. scaber exhibited inhibition rates of lung cancer cell proliferation exceeding 80% at a concentration of 10 µmol·L~(-1), higher than the positive drug paclitaxel. These results indicate that the fingerprint of E. scaber is highly characteristic, and the quantitative analysis method is accurate and stable, providing references for the research on quality standards of E. scaber. Four sesquiterpene lactones in E. scaber show significant anti-cancer activity and can serve as Q-markers for E. scaber.

ArhGAP11A mediates amyloid-ß generation and neuropathology in an Alzheimer's disease-like mouse model.

Amyloid-ß (Aß) plays an important role in the neuropathology of Alzheimer's disease (AD), but some factors promoting Aß generation and Aß oligomer (Aßo) neurotoxicity remain unclear. We here find that the levels of ArhGAP11A, a Ras homology GTPase-activating protein, significantly increase in patients with AD and amyloid precursor protein (APP)/presenilin-1 (PS1) mice. Reducing the ArhGAP11A level in neurons not only inhibits Aß generation by decreasing the expression of APP, PS1, and ß-secretase (BACE1) through the RhoA/ROCK/Erk signaling pathway but also reduces Aßo neurotoxicity by decreasing the expressions of apoptosis-related p53 target genes. In APP/PS1 mice, specific reduction of the ArhGAP11A level in neurons significantly reduces Aß production and plaque deposition and ameliorates neuronal damage, neuroinflammation, and cognitive deficits. Moreover, Aßos enhance ArhGAP11A expression in neurons by activating E2F1, which thus forms a deleterious cycle. Our results demonstrate that ArhGAP11A may be involved in AD pathogenesis and that decreasing ArhGAP11A expression may be a promising therapeutic strategy for AD treatment.

Fc effector of anti-Aß antibody induces synapse loss and cognitive deficits in Alzheimer's disease-like mouse model.

Passive immunotherapy is one of the most promising interventions for Alzheimer's disease (AD). However, almost all immune-modulating strategies fail in clinical trials with unclear causes although they attenuate neuropathology and cognitive deficits in AD animal models. Here, we showed that Aß-targeting antibodies including their lgG1 and lgG4 subtypes induced microglial engulfment of neuronal synapses by activating CR3 or FcγRIIb via the complex of Aß, antibody, and complement. Notably, anti-Aß antibodies without Fc fragment, or with blockage of CR3 or FcγRIIb, did not exert these adverse effects. Consistently, Aß-targeting antibodies, but not their Fab fragments, significantly induced acute microglial synapse removal and rapidly exacerbated cognitive deficits and neuroinflammation in APP/PS1 mice post-treatment, whereas the memory impairments in mice were gradually rescued thereafter. Since the recovery rate of synapses in humans is much lower than that in mice, our findings may clarify the variances in the preclinical and clinical studies assessing AD immunotherapies. Therefore, Aß-targeting antibodies lack of Fc fragment, or with reduced Fc effector function, may not induce microglial synaptic pruning, providing a safer and more efficient therapeutic alternative for passive immunotherapy for AD.

[Exercise regulates lipid metabolism via lipophagy and its molecular mechanisms].

Lipophagy is a kind of selective autophagy, which can selectively identify and degrade lipid droplets and plays an important role in regulating cellular lipid metabolism and maintaining intracellular lipid homeostasis. Exercise can induce lipophagy and it is also an effective means of reducing body fat. In this review, we summarized the relationship between exercise and lipophagy in the liver, pancreas, adipose tissue, and the possible molecular mechanisms to provide a new clue for the prevention and treatment of fatty liver, obesity and other related metabolic diseases by exercise.

[Pollution Characteristic and Control Factor Analysis of Atmospheric Ozone During Summer Typical Periods in Linyi, Shandong].

In June 2020, an observation experiment of O3 and its precursors was carried out in Linyi City, Shandong Province. Based on the observation data and MCM photochemical model simulation, the formation mechanism and control mechanism of an ozone pollution case in mid-June were analyzed. The study found that, despite the high precipitation during the observation period, ozone concentrations rapidly accumulated and exceeded the limits once the weather cleared, with the 1-h average and 8-h φ (O3) exceeding the national ambient air quality standards on 10 days (32% in frequency)and 14 days (45%), respectively. The diurnal variation in O3 concentration was unimodal and accompanied by the afternoon peak at 16:00. MCM simulation results showed that the daily net reaction rate of O3 was 20×10-9 h-1, and HO2·+NO and RO2·(except CH3O2·)+NO contributed 49.0%-51.1% and 37.3%-40.2% of O3 generation, respectively. The contribution of the·OH+NO2 reaction to the total consumption of O3 was 35.1%-57.4%. The results of VOCs reactivity, relative incremental reactivity (RIR), and the EKMA curve method showed that the generation of O3 was more sensitive to alkenes (mainly trans-2-pentene and trans-2-butene)and aromatics (mainly m/p-xylene and toluene)but was negatively sensitive to NOx. In other words, the reduction in VOCs concentration would lead to the decrease in O3 concentration, whereas the reduction in NOx concentration would lead to the increase in O3 concentration. PMF source analysis results showed that volatile sources used by solvents and vehicle exhaust emissions contributed significantly to the above key precursor VOC species. Considering the titration effect of NO from vehicle exhaust emissions on ozone, controlling the use of volatile sources of solvents can realize the control of O3 pollution accurately and efficiently.

Rutin prevents tau pathology and neuroinflammation in a mouse model of Alzheimer's disease.

BACKGROUND: Tau pathology is a hallmark of Alzheimer's disease (AD) and other tauopathies. During disease progression, abnormally phosphorylated forms of tau aggregate and accumulate into neurofibrillary tangles, leading to synapse loss, neuroinflammation, and neurodegeneration. Thus, targeting of tau pathology is expected to be a promising strategy for AD treatment. METHODS: The effect of rutin on tau aggregation was detected by thioflavin T fluorescence and transmission electron microscope imaging. The effect of rutin on tau oligomer-induced cytotoxicity was assessed by MTT assay. The effect of rutin on tau oligomer-mediated the production of IL-1ß and TNF-α in vitro was measured by ELISA. The uptake of extracellular tau by microglia was determined by immunocytochemistry. Six-month-old male Tau-P301S mice were treated with rutin or vehicle by oral administration daily for 30 days. The cognitive performance was determined using the Morris water maze test, Y-maze test, and novel object recognition test. The levels of pathological tau, gliosis, NF-kB activation, proinflammatory cytokines such as IL-1ß and TNF-α, and synaptic proteins including synaptophysin and PSD95 in the brains of the mice were evaluated by immunolabeling, immunoblotting, or ELISA. RESULTS: We showed that rutin, a natural flavonoid glycoside, inhibited tau aggregation and tau oligomer-induced cytotoxicity, lowered the production of proinflammatory cytokines, protected neuronal morphology from toxic tau oligomers, and promoted microglial uptake of extracellular tau oligomers in vitro. When applied to Tau-P301S mouse model of tauopathy, rutin reduced pathological tau levels, regulated tau hyperphosphorylation by increasing PP2A level, suppressed gliosis and neuroinflammation by downregulating NF-kB pathway, prevented microglial synapse engulfment, and rescued synapse loss in mouse brains, resulting in a significant improvement of cognition. CONCLUSION: In combination with the previously reported therapeutic effects of rutin on Aß pathology, rutin is a promising drug candidate for AD treatment based its combinatorial targeting of tau and Aß.

Electric pulse stimulation inhibited lipid accumulation on C2C12 myotubes incubated with oleic acid and palmitic acid.

OBJECTIVE: To investigate the effect of electrical pulse stimulation (EPS) on lipid accumulation and alteration of fatty acid-related enzymes in C2C12 myotubes incubated with fatty acids. METHODS: Mouse C2C12 myotubes were incubated with oleic acid and palmitic acid, and differentiated C2C12 myotubes were treated with EPS, oil-red O (ORO), BODIPY staining and triglyceride (TG) content were examined. Total RNA was isolated, and real-time polymerase chain reaction analysis was performed. RESULTS: (1) EPS decreased TG content (p < .01). (2) EPS significantly induced the mRNA expression of FAD/CD36 (p < .05), FATP4 (p < .001), FABP1 (p < .01) and FABP5 (p < .01). (3) EPS significantly inhibited the mRNA expression of fatty acid synthase (p < .01). (4) Adipose triglyceride lipase and hormone-sensitive lipase expression were significantly elevated (p < .001), and induced the mRNA expression of CPT1 (p < .01), ACOX1 (p < .05), UCP3 (p < .05) and PPARα (p < .001) after EPS. CONCLUSION: EPS reduced lipid droplet accumulation; enhanced CD36, FATP4, FABP1 and FABP5 expression; inhibited C2C12 myotube fatty acid re-esterification; and promoted fatty acid oxidation in C2C12 myotubes.

MYC-regulated lncRNA NEAT1 promotes B cell proliferation and lymphomagenesis via the miR-34b-5p-GLI1 pathway in diffuse large B-cell lymphoma.

BACKGROUND: LncRNA NEAT1 has been identified as a tumour driver in many human cancers. However, the underlying mechanism of lncRNA NEAT1 in diffuse large B-cell lymphoma (DLBCL) progression is unclear. METHODS: The expression levels of NEAT1, GLI1 and miR-34b-5p were detected by RT-qPCR and Western blotting in DLBCL tissues and cell lines. MTT and colony formation assays were performed to examine cell proliferation, while annexin-V staining and TUNEL assays were performed to measure cell apoptosis. The effect of NEAT1, GLI1 and miR-34b-5p on cell cycle-associated proteins was evaluated by Western blotting. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were employed to investigate the interaction between NEAT1 and miR-34b-5p or GLI1 and miR-34b-5p. Moreover, chromatin immunoprecipitation (ChIP) was performed to demonstrate the interaction between MYC and NEAT1. RESULTS: NEAT1 and GLI1 were upregulated while miR-34b-5p was downregulated in DLBCL tissues and cell lines compared to normal controls. Knockdown of NEAT1 or overexpression of miR-34b-5p inhibited cell proliferation but promoted cell apoptosis. Overexpression of NEAT1 reversed GLI1-knockdown induced attenuation of cell proliferation. In other words, NEAT1 acted as a competing endogenous RNA (ceRNA), regulating the miR-34b-5p-GLI1 axis, further affecting the proliferation of DLBCL. Moreover, MYC modulated NEAT1 transcription by directly binding to the NEAT1 promoter. CONCLUSION: We revealed that MYC-regulated NEAT1 promoted DLBCL proliferation via the miR-34b-5p-GLI1 pathway, which could provide a novel therapeutic target for DLBCL.

One-step hydrothermal synthesis of cobalt-vanadium based nanocomposites as bifunctional catalysts for overall water splitting.

Designing low-cost and high-active bifunctional catalysts for overall water splitting has attracted increasing research interest. Herein, the brilliant overall water splitting performance of cobalt-vanadium bimetal-based nanocomposites is explored. Co-V based nanocomposites are synthesized through a one-step hydrothermal method, in which the cobalt species is introduced into the lepidocrocite VOOH and further cobalt vanadium oxide is formed. The additive level of cobalt is optimized and the corresponding effect on electrocatalytic activity is also investigated in this work, systematically. The targeted catalyst (denoted as Co0.2-VOOH) exhibits a unique sheet-like morphology, resulting in the high exposure of catalytically active sites. When used as the bifunctional catalyst, Co0.2-VOOH can achieve a current density of 10 mA cm-2 at the overpotentials of 210 mV for water oxidation and 130 mV for hydrogen generation, respectively. Notably, it only requires low cell voltages of 1.57 and 1.74 V to drive the catalytic current densities of 10 and 100 mA cm-2 during the water splitting process. This work significantly indicates that cobalt-vanadium based materials are promising alternatives for overall water splitting.

Vascular endothelial growth factor B inhibits lipid accumulation in C2C12 myotubes incubated with fatty acids.

To investigate (1) the effect of vascular endothelial growth factor B (VEGFB) on lipid accumulation and the alteration of fatty acids and fatty acid-related enzymes in C2C12 myotubes incubated with fatty acids and (2) the regulatory effect of VEGFB on skeletal muscle lipid metabolism. Mouse C2C12 myotubes were incubated with oleic acid (OA) and palmitic acid (PA), and differentiated mature C2C12 myotubes were treated with VEGFB. Oil-red O staining, BODIPY staining and cell triglycerides (TG) content were examined. Total RNA was isolated, and real-time PCR analysis was performed. Treatment with 100 µM OA and 50 µM PA induced lipid droplet accumulation and increased TG content (p < .01), and 100 ng/mL VEGFB reduced lipid droplet accumulation and decreased TG content (p < .01). Treatment with 100 ng/mL VEGFB significantly induced the mRNA expression of fatty acid transport protein 1 (FATP1) (p < .01) and FATP4 (p < .01). Treatment with 100 ng/mL VEGFB significantly induced the mRNA expression of adipose TG lipase and hormone-sensitive lipase (p < .01) as well as carnitine palmitoyltransferase I (p < .01), peroxisome proliferator-activated receptor-γ coactivator-1α (p < .01), acyl-coa dehydrogenase very long chain (p < .05), acyl-coa synthetase long-chain family member 1 (p < .01), peroxisomal acyl-coenzyme A oxidase 1 (p < .05), and mitochondrial uncoupling protein 3 (p < .01). VEGFB enhanced FATP1and FATP4 expression, promoted C2C12 myotube fatty acid oxidation and TG decomposition, and inhibited C2C12 myotube fatty acid re-esterification, thus inhibiting lipid accumulation in C2C12 myotubes incubated with fatty acids.

Self-Interconnected Porous Networks of NiCo Disulfide as Efficient Bifunctional Electrocatalysts for Overall Water Splitting.

Electrochemical splitting of water has been viewed as a highly efficient technique to produce clean hydrogen and oxygen energy. However, designing inexpensive multifunctional electrocatalysts with high performance is a great challenge. Here, a unique three-dimensional catalyst of self-interconnected porous Ni-Co disulfide networks grown on carbon cloth [(Ni0.33Co0.67)S2 nanowires (NWs)/CC] was prepared by a facile hydrothermal method coupled with further low-temperature sulfuration strategy. As a bifunctional electrocatalyst, (Ni0.33Co0.67)S2 NWs/CC exhibits a remarkable activity to catalyze both hydrogen evolution reaction (HER) and oxygen evolution reaction (OER). To drive a current density of 100 mA cm-2, (Ni0.33Co0.67)S2 NWs/CC needs the overpotentials of 156 mV in 0.5 M H2SO4 solution and 334 mV in 1.0 M KOH solution for HER, respectively. Moreover, when used as a catalyst of OER, (Ni0.33Co0.67)S2 NWs/CC needs an overpotential of 295 mV to produce a current density of 100 mA cm-2. The excellent electrochemical properties are mainly attributed to the synergetic catalysis of a Ni-Co-based bimetallic disulfide, the porous network structure, and the high conduction of CC. Moreover, the two-electrode alkaline water-splitting system constructed by (Ni0.33Co0.67)S2 NWs/CC only needs a low cell voltage of 1.57 V to approach 10 mA cm-2. This work offers more new insights for the design and preparation of the non-noble metal catalysts based on transition metal sulfides with excellent electrocatalytic performance in overall water splitting.

Layered Aggregation with Steric Effect: Morphology-Homogeneous Semiconductor MoS2 as an Alternative 2D Probe for Visual Immunoassay.

Liquid-phase exfoliation routes unavoidably generate 2D nanostructures with inhomogeneous morphologies. Herein, thickness-dependent sorting of exfoliated nanostructures is achieved via a treatment of differential-zone centrifugation in the surfactant aqueous phase. With this approach, homogeneous MoS2 nanosheets are obtained, and due to the intrinsic semiconducting characteristics, those 2D nanosheets are endowed with desired optical properties, rivaling classic gold nanoparticles in sensing applications. Furthermore, MoS2 nanosheets with high uniformity and chemical inertness are coupled with proteins, exhibiting high performance in stability and anti-interferences for bioanalysis. As a consequence of aggregation-induced steric effect, distinguishing running shifts of antibody-anchored conjugates in gel electrophoresis are visually responsive to those specific antigens. This assay enables the easy and fast monitoring of tumor biomarkers just according to "naked-eye" identification of band location in electrophoresis results, which are presented by an alternative visual probe of 2D MoS2 -protein conjugates. The developed visual immunoassay with the synergistic effect of gel electrophoresis techniques and 2D semiconductors pushes significant progress in "home-made" tests for disease early diagnosis.

Fabrication of Pt/Cu3(PO4)2 ultrathin nanosheet heterostructure for photoelectrochemical microRNA sensing using novel G-wire-enhanced strategy.

Herein, we focus on preparing a highly efficient photocatalytic material to construct a signal-on photoelectrochemical (PEC) sensing platform in view of the rigorous demand of accurate miRNA quantification. The well-dispersed Pt nanoclusters-coated copper phosphate ultrathin nanosheets (PtNCs/Cu3(PO4)2NSs) were first successfully synthesized as a photoelectrode material. Because of the ultrathin two-dimensional lamellar structure of Cu3(PO4)2NSs with a 1.3 nm thickness, as well as the homogeneous size and abundant PtNCs loaded on Cu3(PO4)2NSs, the resultant PtNCs/Cu3(PO4)2NSs were employed as a photoelectrode material for the first time and revealed outstanding photocatalytic activity in PEC sensing as a substrate. As a well-designed protocol, we realized accurate miRNA quantification via a novel signal amplification strategy based on G-wire superstructure exponentially ligating a signal probe, which possesses efficient and simple operation compared to the traditional amplification method. Moreover, the electron donor is generated in situ by lactate oxidase (Lox) labels catalyzing lactate for H2O2 production, boosting the efficient separation of electron-hole pairs for further signal amplification. Impressively, this PEC sensing platform is commendably utilized to determine miRNA-141 from prostate carcinoma cell line 22Rv1. This study, considering the excellent PtNCs/Cu3(PO4)2NSs combined with G-wire superstructure for exponential signal amplification strategy, paves a new path in biosensing and clinical diagnosis.

[The characteristics of frequency distribution of KIR2DL1 alleles polymorphism and recognition HLA-C ligand in the Chinese Han population].

OBJECTIVE: To find out the distributed characteristics of KIR2DL1 alleles frequencies and the recognition HLA-C ligand in the Chinese Han population. METHODS: The 111 patients and 116 donors from CMDP were performed the KIR2DL1 high-resolution typing and KIR genotyping using sequence-based testing (SBT) and PCR-SSP methods. RESULTS: A total of 224 individuals with KIR2DL1 locus was predominantly observed and accounted for 98.68% (224/227). There were 3 different KIR2DL1 alleles, including KIR2DL1*00302, *00201 and *00401 alleles polymorphism. The most common phenotype observed were KIR2DL1*00302 (84.82%, 380/448), KIR2DL1*00201 (12.05%, 54/448) and KIR2DL1*00401(3.13%,14/448), present at allele genotype frequencies of 61.04%,6.22% and 1.58% respectively. The allele homozygotic types of KIR2DL1*00302 and KIR2DL1*00302 were the most frequent in 6 KIR2DL1 allele by high resolution typing. The allele heterozygous types of KIR2DL1*00302 and KIR2DL1*00401 presented statistically different in haplotypes A/A and B/x (P=0.001), and KIR2DL1*00401 lacked of all A/A haplotype. The KIR2DL1*00302 and KIR2DL1*00201 allele had significant positive associations between different KIR pairs of KIR2DS1, KIR2DL3, KIR2DS4 and KIR3DL1/S1 using linkage disequilibrium analysis (P<0.01), respectively. In the receptor-ligand of KIR/HLA model after allo-HSCT, KIR2DL1*00302 alleles correlated with their HLA-C2 group ligands. KIR2DL1*00302 and HLA-C*06:02 was the most common combination ligand model, but KIR2DL1*00302 and HLA-C*01:02 was the most frequent mismatch ligand model with the development of NK cell-induced alloreactivity, meanwhile there was statistically significant difference of frequency distribution (P<0.05). CONCLUSION: The KIR2DL1*00302 was the most frequent allele in Chinese Han population. The KIR2DL1 high resolution typing would be beneficial for predicting donor NK cells all activity after hematopoietic stem cell transplantation and selecting suitable donors.