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Li Dong,1 Yu-Min Zheng,2 Xiao-Guang Luo,3 Zhi-Yi He2 1Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, People’s Republic of China; 3Department of Neurology, The First Affiliated Hospital of South University of Science and Technology, The Second Clinical College of Jinan University, Shenzhen People’s Hospital, Shenzhen, People’s Republic of ChinaCorrespondence: Xiao-Guang LuoDepartment of Neurology, The First Affiliated Hospital of South University of Science and Technology, The Second Clinical College of Jinan University, Shenzhen People’s Hospital, Shenzhen, People’s Republic of ChinaEmail guanche537@126.comZhi-Yi HeDepartment of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, People’s Republic of ChinaEmail yizizhan40559@163.comBackground: Parkinson’s disease is a common neurodegenerative disease in the elderly. The incidence of various cancers in Parkinson’s disease patients is significantly lower than in healthy people. Parkinson’s disease patients are individuals with a high tendency for inflammation, whose peripheral immune system is represented in an activated state. We hypothesized that the hyperinflammatory predisposition of Parkinson’s disease patients is pathogenic.Methods: DBA/1 mice were used to simulate “highly inflammatory individuals”, and the carcinogen DEN was used to induce malignancy. Hematoxylin & eosin (H&E) staining was used to observe the formation of lung tumors. Apoptosis of neurons was observed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Immunohistochemistry and flow cytometry were used to observe CD4, CD28, major histocompatibility complex II (MHCII), cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), and programmed death 1 (PD-1). The ionized calcium binding adaptor molecule-1 (IBA-1) + inducible nitric oxide synthase (iNOS) was used to label M1 microglia, and IBA-1 + arginase 1 (Arg1) was used to label M2 microglia by immunofluorescence. The expression of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and anti-inflammatory cytokines IL-10 and IL-4 was detected by ELISA.Results: DBA/1 mice with high inflammatory tendency showed a continuous increase of peripheral inflammation, promoting intracranial inflammation, decreasing the tumor incidence and increasing the neurodegeneration under induction of malignant change. CD28 and CTLA-4/PD-1 reduced the T-cell-dominated inflammatory response, reduced the intracerebral inflammatory response, protected from neurodegeneration, and increased the incidence of tumor. Combination of CTLA-4 and PD-1 blocker can overactivate T cells, worsen peripheral and intracranial inflammation, reduce the incidence of tumor, cause damage to dopamine neurons, and promote the occurrence of neurodegeneration.Conclusion: High inflammatory tendency induced by malignant stimulation through the imbalance of CD28 and CTLA-4/PD-1 leads to dopamine neuron injury.Keywords: high inflammatory tendency, malignant stimulation, CD28, CTLA-4/PD-1, dopamine neuron injury

In this study, we investigated the beneficial effects of high endogenous levels of n-3 polyunsaturated fatty acids (PUFAs) on skeletal muscle repair and regeneration using a mouse cardiotoxin (CTX, 20 μM/200 μL) -induced gastrocnemius muscle injury model. Transgenic fat-1 mice expressing the Caenorhabditis elegans fat-1 gene, encoding n-3 fatty acid desaturase, showed higher n-3 PUFA levels and lower n-6/n-3 PUFA ratios in gastrocnemius muscle tissues. Hematoxylin and eosin and Masson’s trichrome staining of gastrocnemius sections revealed increased muscle fiber size and reduced fibrosis in fat-1 mice on days 7 and 14 after CTX injections. Gastrocnemius muscle tissues from fat-1 mice showed reduced inflammatory responses and increased muscle fiber regeneration reflecting enhanced activation of satellite cells on day 3 after cardiotoxin injections. Gastrocnemius muscle tissues from cardiotoxin-treated fat-1 mice showed reduced levels of pro-apoptotic proteins (Caspase 3 and Bax) and increased levels of anti-apoptotic proteins (Bcl-2 and Survivin). Moreover, eicosapentaenoic acid (EPA) reduced the incidence of apoptosis among cardiotoxin-treated C2C12 mouse myoblasts. These findings demonstrate that higher endogenous n-3 PUFA levels in fat-1 mice enhances skeletal muscle repair and regeneration following cardiotoxin-induced injury.

Background The global incidence and mortality rates of liver cancer, which is the second leading cause of cancer-related deaths worldwide, are increasing. However, information on its epidemiology and clinical prognosis is limited. This study aimed to characterize the epidemiology and prognostic factors of secondary liver cancer to aid in the pretreatment evaluation of the disease. Methods Patients diagnosed with secondary liver cancer between 2010 and 2014 in the Surveillance, Epidemiology, and End Results (SEER) database were retrospectively included. Kaplan-Meier analysis and Multivariate Cox regression analysis were performed to screen for significant factors associated with secondary liver cancer. Results A total of 85,738 secondary liver cancer patients were identified; in this population, the first primary site was the lung (25.9%), followed by the colorectum, pancreas, stomach, breast, and cecum. Patients with primary tumors of the colorectum, cecum and breast had longer median survival time. Advanced age, male gender, black race, poor differentiation or lack of differentiation, regional lymph node metastases, and presence of distant metastasis were associated with poor prognosis. Conclusions In this study, novel findings on the role of the primary site and synchronous distant metastasis to specific organs in patients with secondary liver cancer were described. These findings have significant implications in clinical diagnosis and treatment, and provide a better understanding of secondary liver cancer in the general population.

Osteoarthritis (OA) is a common articular ailment presented with cartilage loss and destruction that is common observed in the elderly population. Physalin A (PA), a natural bioactive withanolide, exerts anti-inflammatory residences in more than a few diseases; however, little is known about its efficacy for OA treatment. Here, we explored the therapeutic effects and potential mechanism of PA in mouse OA. After the in vitro administration of PA, the expression of inflammation indicators including inducible nitric oxide synthase and cyclooxygenase-2 was low, indicating that PA could alleviate the IL-1β-induced chondrocyte inflammation response. Moreover, PA reduced IL-1β-induced destruction of the extracellular matrix by upregulating the gene expression of anabolism factors, including collagen II, aggrecan, and sry-box transcription factor 9, and downregulating the gene expression of catabolic factors, including thrombospondin motif 5 and matrix metalloproteinases. In addition, the chondroprotective effect of PA was credited to the inhibition of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways. Furthermore, in vivo experiments showed that intra-articular injection of PA could alleviate cartilage destruction in a mouse OA model. However, the anti-inflammatory, anabolism enhancing, catabolism inhibiting, and MAPK and NF-κB signaling pathway inhibiting properties of PA on IL-1β-induced chondrocytes could be reversed when integrin αVβ3 is knocked down by siRNA. In conclusion, our work demonstrates that PA exhibits a chondroprotective effect that may be mediated by integrin αVβ3. Thus, PA or integrin αVβ3 might be a promising agent or molecular target for the treatment of OA.

Lung and systemic inflammation are associated with impaired lung function and increased mortality in patients with chronic obstructive pulmonary disease (COPD). Theophylline and glucocorticoids have been shown to have an anti-inflammatory effect in some respiratory diseases. However, corticosteroid insensitivity is a major barrier to the anti-inflammatory management of COPD. This study aimed to explore whether a combined treatment of theophylline and dexamethasone (Dex) could decrease cigarette smoke extract (CSE)-induced inflammation via prevention of a reduction in histone deacetylase 2 (HDAC2) expression and through inhibition of the PI3K/Akt pathway, which may be related to corticosteroid sensitivity. The half-maximal inhibitory concentration (IC(50)) of Dex (IC(50)-Dex) was used to as a marker of corticosteroid sensitivity. IC(50)-Dex was determined through observation of Dex inhibition of tumor necrosis factor-α (TNF-α)-induced interleukin (IL)-8 release. Using reverse transcription quantitative PCR and western blotting, U937 cells treated with CSE were assessed for HDAC2 expression levels and phosphorylation levels of Akt. Theophylline and Dex pre-treatment was shown to significantly reduce the CSE-induced release of IL-8 and TNF-α. The combination of theophylline and Dex pretreatment also reversed corticosteroid insensitivity in CSE-induced U937 cells and inhibited the PI3K/AKT pathway to a greater extent than theophylline treatment alone. CSE-treated U937 cells showed a reduction in HDAC2 mRNA and protein expression compared with the control group. However, this effect was reduced after pre-incubation with the combined therapy or theophylline alone. In conclusion, pretreatment with theophylline and Dex decreased CSE-induced inflammation via inhibition of the PI3K/Akt pathway and increase in HDAC2 protein expression.

Objectives. Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the loss of midbrain dopaminergic neurons in the substantia nigra. The present study investigated miR-141-3p/sirtuin1 (SIRT1) activity in a 1-methyl-4-phenylpyridinium- (MPP+-) induced PC12-cell model of PD. Methods. PC12 cells were exposed to MMP+ following induction of differentiation by nerve growth factor (NGF). miR-141-3p and SIRT1 expressions were examined using RT-qPCR and western blot. Cell viability was evaluated using the MTT assay. Apoptosis percentage, reactive oxygen species (ROS) production, and mitochondrial membrane potential (Δψm) were evaluated using flow cytometry. Expression of Nuclear factor-kappa B- (NF-κB-) related proteins was determined by western blot. Bioinformatic analysis, RT-qPCR, and luciferase reporter assay were used to confirm the interaction between miR-141-3p and SIRT1. Results. miR-141-3p was upregulated, and SIRT1 was downregulated in MPP+-treated PC12 cells. MPP+ treatment also upregulated nitric oxide synthase 1 (Nos1) and α-synuclein. miR-141-3p induced apoptosis, oxidative stress, mitochondrial dysfunction, and downregulated the SIRT1 mRNA expression. The luciferase reporter assay showed that SIRT1 was the target of miR-141-3p. SIRT1 transfection attenuated apoptosis, ROS production and maintained Δψm. SIRT1 also downregulated Nos1, tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), interleukin 6(IL-6) and upregulated B cell lymphoma 2 (Bcl-2) protein. In addition, SIRT1 activator resveratrol blocked the effects of miR-141-3p mimic on Nos1, α-synuclein, and mitochondrial membrane potential. SIRT1 inhibitor sirtinol reversed the biological effects of miR-141-3p. Conclusion. Increased miR-141-3p induced apoptosis, oxidative stress, and mitochondrial dysfunction in MPP+-treated PC12 cells by directly targeting the SIRT1 expression. Our study provided a potential therapeutic strategy for PD.

Parkinson's disease (PD) is a common neurodegenerative disorder, which is characterized by the selective and progressive death of dopaminergic (DA) neurons in the substantia nigra. Increasing evidence suggests that inflammation is important in the degeneration of DA neurons. The purinergic receptor subtype P2X7 receptor (P2X7R) is key in the activation and proliferation of microglia. The present study aimed to examine whether inhibiting purinergic P2X7 receptors is neuroprotective in a rat model of PD, specifically via inhibiting p38 mitogen‑activated protein kinase (MAPK). In an intranigral lipopolysaccharide (LPS) rat model of PD, immunohistochemical analysis revealed enhanced expression of P2X7R was observed in microglia. The administration of the P2X7R antagonist, brilliant blue G (BBG), reduced activation of the microglia and the loss of nigral DA neurons. In addition, immunohistochemistry and western blot analysis revealed the phosphorylation level of p38 MAPK increased in the microglia of the LPS‑injected rats, which was inhibited by BBG treatment. The p38 MAPK inhibitor, SB203580, reduced microglial activation and the loss of DA neurons. Thus, these findings suggested that inhibition of P2X7R by BBG attenuated microglial activation and the loss of substantia nigra DA neurons via p38 MAPK in the rat LPS model of PD.

The present study aimed to investigate the effects of the phosphoinositide 3‑kinase (PI3K)/Akt signaling pathway on the Wnt/β‑catenin signaling pathway in rats with focal cerebral ischemia‑reperfusion injury. A total of 96 rat focal cerebral ischemia‑reperfusion models, established according to a modified version of Longa's method, were randomly divided into four groups: Sham‑operated (S), cerebral ischemia‑reperfusion injury (I), cerebral ischemia‑reperfusion + basic fibroblast growth factor (bFGF) post‑processing and, finally, cerebral ischemia‑reperfusion + bFGF post‑processing + PI3K inhibitor LY294002 (LY). Each group consisted of 24 rats and each group was divided into four subgroups according to the indicated reperfusion times of 12, 24, 48 and 72 h. The morphological changes of the cortical tissue and the cellular apoptosis were determined using hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling method, respectively. The expression levels of phosphorylated (p‑)Akt, glycogen synthase kinase‑3β (GSK‑3β) mRNA and β‑catenin in the cortical tissue were detected at different time‑points. The number of apoptotic cells and the expression levels of p‑Akt, GSK‑3β mRNA and β‑catenin in the I and LY groups were significantly higher compared with those in the S group (P

Given that cyclooxygenase-2 (COX-2) plays a crucial role during cerebral ischemia and Apobec-1 is a critical regulator of COX-2 mRNA stabilization in gastrointestinal settings, the correlation of COX-2 and Apobec-1 was investigated in neurogenic cells and rat model of cerebral ischemia. After neurogenic SH-SY5Y, NG108-15 and PC12 cells were exposed to oxygen-glucose deprivation, cell viability, LDH leakage and Apobec-1 expression were determined. The effect of Apobec-1 overexpression on injury severity of oxygen-glucose deprivation, COX-2 expression, C-to-U editing of COX-2 mRNA were measured in vitro. Then the correlation of Apobec-1 level and injury severity was analyzed in cells with oxygen-glucose deprivation and in rats with middle cerebral artery occlusion. Apobec-1 expression was elevated along with upregulation of COX-2 and injury severity of oxygen-glucose deprivation in the three cell lines. Apobec-1 overexpression aggravated injury of oxygen-glucose deprivation in vitro and could be correlated to injury severity in vivo. Meanwhile, Apobec-1 increased COX-2 expression and COX-2 mRNA stabilization in neurogenic cells, and failed to catalyze C-to-U editing of COX-2 mRNA. Apobec-1 could upregulate COX-2 expression in neurogenic cells by stabilizing COX-2 mRNA, and might aggravate injury of oxygen-glucose deprivation in neurogenic cells as well as in rats with cerebral ischemia.

Background: Macrolide antibiotics have anti-inflammatory effects which are utilized for the treatment of chronic inflammatory airway diseases. Recently, their anti-inflammatory effects have been proposed to be beneficial in patients with chronic obstructive pulmonary disease (COPD). Objectives: Since the molecular mechanisms of anti-inflammatory effects are associated with inhibition of activator protein 1 (AP-1) and nuclear factor (NF)-ĸB, and both are reported to be involved in the expression of γ-glutamylcysteine synthetase (γ-GCS), we set out to determine if these drugs influence the oxidant-antioxidant balance in human bronchial epithelial (HBE) cells. Methods: 16HBE cells were preincubated with erythromycin (EM) at different concentrations and times and then exposed to hydrogen peroxide (0.01 mM). Levels of interleukin (IL)-8 and glutathione (GSH), and activity of γ-GCS and γ-GCS heavy subunit (γ-GCS-HS) protein production were assayed. AP-1 and NF-ĸB binding to the 5′-flanking region of IL-8 and γ-GCS-HS genes was assessed by electrophoretic mobility-shift assay. Results: The increase in IL-8 levels and activity of AP-1 induced by H2O2 were abrogated by preincubation of the cells with EM (5 µg/ml) for 36 h. We also showed that preincubation with EM for 48 h inhibited H2O2-induced GSH levels, γ-GCS activity and expression of γ-GCS-HS, and decreased AP-1 binding to the γ-GCS-HS 5′-flanking region. Conclusions: The confirmation of antioxidants maintaining enzyme suppression by EM raised concerns on whether this drug could disrupt the oxidant/ antioxidant balance during long-term use. These data provide important insights into the treatment of inflammatory lung diseases with macrolide antibiotics.

Phorbol myristate acetate (PMA), as a potent tumor promoter, may induce microglial senescence. The present study investigated the effect of PMA infection on microglial senescence. From 58 male Sprague‑Dawley rats, 10 were randomly selected and divided into a PMA injection group, containing five rats (0.5 µg/µl PMA) and a control group, containing five rats (commensurable 0.9% saline). Immunofluorescent staining of Iba‑1 and enzyme‑linked immunosorbent assay analyses of the expression levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑1 β were performed in these two groups. The remaining 48 rats were randomly divided into the following three groups, each containing 16 rats: Repeated injection control group (commensurable normal saline, once a week for 4 weeks), single PMA injection group (0.5 µg/µl PMA, once in the first week) and repeated injection PMA group (0.5 µg/µl PMA, once a week for 4 weeks). The expression levels of p21, detected using double immunofluorescence staining with Iba‑1, and β‑galactosidase, via double immunohistochemical staining of Iba‑1, were examined in these three groups. The results indicated that a single injection of PMA did not change the microglial morphology and had no significant effects on the expression levels of TNF‑α and IL‑1β, compared with the control group (P>0.05). Following four repeated injections of PMA, the microglia in the substantia nigra presented with features of senescence, characterized by increased expression levels of β-galactosidase (P

Objective To clarify the relationship between the quantitatively assessed cube-copying test (CCT) and clinical profiles of cognitive and motor ability in Chinese patients with Parkinson disease (PD). Methods We gave the Montreal Cognitive Assessment (MoCA), which includes the CCT, to evaluate the cognitive function of 102 outpatients with PD. We also gave the Unified Parkinson's Disease Rating Scale (UPDRS) II and III and the Hoehn-Yahr scale to evaluate the patients' motor function and disease severity, respectively. We used Maeshima's method for quantitative assessment of the CCT, and calculated CCT errors by adding incomplete connections and plane-drawing errors. We divided the patients into 2 groups based on normal (no errors) versus abnormal (≥1 errors) CCT scores. Results We found 34 patients with normal scores and 68 with abnormal scores. The 2 groups had significant differences in age of onset, MoCA score, UPDRS II and III scores, and cognitive deterioration rate. CCT errors correlated inversely with cognitive domains except for orientation. Executive function was most commonly affected in both groups. We found correlations between numbers of CCT errors and left-limb movement, fine hand movement, postural instability and gait disorders, UPDRS II and III scores, and cognitive and motor deterioration rates. Conclusions The quantitatively assessed CCT may be useful in estimating cognitive and motor dysfunction in patients with PD, and in monitoring disease progression.

The relation between the LRRK2 mutation and its effect on Parkinson’s disease (PD) has always caught a lot attention. Recent studies found that the G2385R polymorphism of LRRK2 may increase the risk of PD in Asian populations. Here we tried to clarify the relationship between the LRRK2 G2385R variant and the clinical profiles including motor complication in Chinese PD patients. We identified the LRRK2 variant in the Chinese Han population in northern China and evaluated the relationship between the G2385R variant and clinical profiles through comparison between 36 carriers and 139 non-carriers. We found that G2385R carriers scored significantly higher in motor fluctuation and dyskinesia than non-carriers. Logistic regression analysis showed that the G2385R variant was an independent risk factor for motor fluctuation in females (odds ratio = 12.538, 95 % CI 2.216–70.942, P = 0.004), and a Chi-squared test showed that the frequency of dyskinesia tended to be higher in the carrier group compared to the non-carrier group (16 vs. 4.4 %, P = 0.050, OR = 4.127, 95 % CI 1.074–15.864). These findings indicate that the variant was closely related to the occurrence of motor complication. Additionally, the G2385R variant was significantly related to the early-onset of PD in female carriers (20.0 vs. 1.5 %, odds ratio = 16.25, 95 % CI 1.557–169.618, P = 0.020). Our study found that the G2385R variant was significantly associated with motor complications and that this variant was an independent risk factor for motor fluctuation in females. These findings provide the necessary preliminary data to better understand the unique profile of PD G2385R variant carriers.

Background We performed a meta-analysis to evaluate the role of 18 F-fluorodeoxyglucos -e positron emission tomography/computed tomography ( 18 FDG-PET/CT) in detecting mediastinal nodal metastasis in patients with non-small cell lung cancer (NSCLC). Methods Studies about 18 FDG-PET/CT for detecting mediastinal nodal metastasis in patient with NSCLC were systematically searched in the MEDLINE, EMBASE, and EBM Review databases from January 1, 2000 to July 26, 2011. A software called "Meta-Disc" was used to obtain pooled estimates of sensitivity, specificity, positive likelihood ratio (PLR), and negative likelihood ratio (NLR), respectively. We also calculated summary receiver operating characteristic (SROC) curves, and the Q* index. Results 20 articles fulfilled all inclusion criteria (3028 eligible patients). The pooled sensitivity, and specificity with 95% confidence interval for PET/CT on a per-patient analysis were 0.719 (0.683–0.753), and 0.898 (0.882–0.912). Corresponding values for PET/CT on a per-nodal-station analysis were 0.610 (0.582–0.636), 0.924 (0.918–0.930). The Q* index estimates under SROC were 0.8464 and 0.8067, respectively. Conclusions 18 FDG-PET/CT had more specificity but less sensitivity for mediastinal nodal metastasis in patients with NSCLC.

Background and Aim: The dual action of microglia in neurodegenerating diseases has been controversial for some time. Recent studies indicate that microglia senescence might be the key determinant. When microglia age, they function abnormally and fail to respond correctly to stimuli, which eventually promotes neurodegeneration. Accumulating evidence has shown a close relationship between inflammation and aging. Since neuroinflammation is characterized by microglia activation, we assessed if the repeated activation of microglia would lead to senescence. Method: The microglia cell line BV2 was repeatedly stimulated every 48 h with lipopolysaccharide (LPS; 10 ng/ml) and senescence was evaluated by β-galactosidase staining and the presence of senescence-associated heterochromatic foci as well as by cell cycle arrest detection by flow cytometry. The senescence-associated protein p53 was also detected by Western blot. Results: β-Galactosidase staining was barely detectable in control cells, while it tended to increase with repeated LPS stimulation and was positive in most cells after stimulation with LPS 6 times. Similarly, senescence-associated heterochromatic foci were most prominent in cells repeatedly stimulated with LPS, while almost undetectable in control cells or cells receiving a single stimulation. p53 expression was highest in the cells that received LPS stimulation 6 times, and the largest number of cells arrested in the G0/G1 phase was observed in this same group. Conclusion: Microglial cells tend to undergo senescence after repeated activation, implying that microglia senescence may start after multiple inflammatory challenges.

Background/Aims: Cognitive impairment (CI) is common in Parkinson’s disease (PD), and the cognitive deterioration rate (CDR) is heterogeneous among PD patients. However, very few studies have reported on the association of PD features and risk factors with rapid CDR. The Montreal Cognitive Assessment (MoCA) is considered to be a sensitive and reliable approach to detect mild CI. In the present study, we sought to define and compare the cognitive profiles and clinical features of PD patients with slow or rapid CDRs, and then to identify the PD risk factors associated with rapid CDR. Methods: A cross-sectional study of cognitive rate was performed using the MoCA in a cohort of 73 PD patients and 41 controls matched for age, sex and education level. Results: The rapid CDR group was characterized by older age (58.8 years in slow CDR vs. 64.1 in rapid CDR; p = 0.02), later age at disease onset (52.7 vs. 61.7 years; p < 0.001), a faster deterioration rate of movement symptoms (UPDRS III increment of 12.8 vs. 5.9/year; p < 0.001), a higher rate in multiple-domain CI (38.9 vs. 10.8%), and generally lower MoCA subscores for the Clock Drawing Test, attention, verbal fluency and abstraction. According to the univariate logistic regression model, onset age, movement deterioration rate, multiple domains CI and executive function CI were risk factors for rapid CDR. However, only the movement deterioration rate (p = 0.01) and onset age (p = 0.05) remained independent predictors for rapid CDR according to the multivariate logistic regression model. Conclusions: The CI deterioration in a subset of PD patients appears to progress more rapidly. Identifying those PD patients may not only help to predict the development of PD dementia, but also facilitate therapeutic intervention at early disease stages.

Background CYP4F2 is a member of the cytochrome P450 enzymes and is responsible for metabolizing arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE); 20-HETE plays a role in the regulation of vascular tone in the cerebral, coronary, and renal circulation. The present study aimed to evaluate whether or not the CYP4F2 gene polymorphism V433M (rs2108622) is involved in ischemic stroke in the Northern Chinese Han population. Methods In a case–control study, the participants included 302 (193 males and 109 females) patients with ischemic stroke and 350 (212 males and 138 females) healthy subjects. The V433M polymorphism of the CYP4F2 gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) with the restriction enzyme PvuII. Results The frequencies of the GG genotype and the G allele were higher in participants with ischemic stroke than in the control group ( P = 0.018). Multiple logistic regression analysis revealed the significance of the rs2108622 in males after adjustment for confounding factors. No difference was found in all participants and females. Conclusion The GG genotype and G allele were associated with ischemic stroke in the male Northern Chinese Han population.