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Background: The mechanism by which low androgen status inhibit erectile function has not yet been clearly elucidated. Neurogranin (Ng) is a Ca 2+ -sensitive calmodulin binding protein that is expressed in endothelial cells and regulates eNOS function., Objectives: To investigate whether low androgen status inhibit erectile function by regulating the Ng/CaN/AKT/eNOS pathway in the penile cavernous tissue of rats., Materials and Methods: Thirty-six 8-week-old male Sprague-Dawley rats were randomly divided into six groups as follows (n = 6): 4-week control group (4w-control), 4-week castration group (4w-cast), 4-week castration+testosterone replacement group (4w-cast+T), 8-week control group (8w-control), 8-week castration group (8w-cast), and 8-week castration+testosterone replacement group (8w-cast+T). Four weeks and eight weeks after surgery, the ratio of the maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP) was examined. The level of NO and the expression of Ng, calcineurin (CaN), AKT, p-AKT(S473), eNOS, and p-eNOS(Ser1177) in the penile cavernous tissue of each group were determined., Results: Ng and CaN were mainly expressed in the membrane and cytoplasm of endothelial cells and smooth muscle cells in the penile cavernous tissue of rats. The ICPmax/MAP and the concentration of NO in the cast group were significantly lower than those in the control group and cast+T replacement group (p < 0.01). The expression of Ng and the ratios of p-AKT/AKT and p-eNOS/eNOS in the penile cavernous tissue of rats in the cast group were significantly lower than those in the control group and cast+T replacement group (p < 0.01). The expression of CaN in the penile cavernous tissue of rats in the cast group was significantly increased compared with that in the control group and the cast+T replacement group (p < 0.01)., Conclusion: Inhibiting the expression of Ng and subsequently upregulating the expression of CaN in the rat penile cavernous tissue was one of the upstream mechanisms of low androgen status inhibiting erectile function by inhibiting the AKT/eNOS signaling pathway., (© 2022 American Society of Andrology and European Academy of Andrology.)

Aims: Secondary gliosarcoma (SGS) rarely arises post treatment of primary glioblastoma multiforme (GBM), and contains gliomatous and sarcomatous components. The origin and clonal evolution of SGS sarcomatous components remain uncharacterized. Therapeutic radiation is mutagenic and can induce sarcomas in patients with other tumor phenotypes, but possible causal relationships between radiotherapy and induction of SGS sarcomatous components remain unexplored. Herein, we investigated the clonal origin of SGS in a patient with primary GBM progressing into SGS post-radiochemotherapy., Methods: Somatic mutation profile in GBM and SGS was examined using whole-genome sequencing and deep-whole-exome sequencing. Mutation signatures were characterized to investigate relationships between radiochemotherapy and SGS pathogenesis., Results: A mutation cluster containing two founding mutations in tumor-suppressor genes NF1 (variant allele frequency [VAF]: 50.0% in GBM and 51.1% in SGS) and TP53 (VAF: 26.7% in GBM and 50.8% in SGS) was shared in GBM and SGS. SGS exhibited an overpresented C>A (G>T) transversion (oxidative DNA damage signature) but no signature 11 mutations (alkylating-agents - exposure signature). Since radiation induces DNA lesions by generating reactive oxygen species, the mutations observed in this case of SGS were likely the result of radiotherapy rather than chemotherapy., Conclusions: Secondary gliosarcoma components likely have a monoclonal origin, and the clone possessing mutations in NF1 and TP53 was likely the founding clone in this case of SGS., (© 2021 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)

Aims: High immune cell infiltration in gliomas establishes an immunosuppressive tumor microenvironment, which in turn promotes resistance to immunotherapy. Hence, it is important to identify novel targets associated with high immune cell infiltration in gliomas. Our previous study showed that serum levels of beta-2 microglobulin (B2M) in lower-grade glioma patients were lower than those in glioblastoma patients. In the present study, we focused on exploring the roles of B2M in glioma immune infiltration., Methods: A large cohort of patients with gliomas from the TCGA, CGGA, and Gravendeel databases was included to explore differential expression patterns and potential roles of B2M in gliomas. A total of 103 glioma tissue samples were collected to determine the distributions of B2M protein levels by immunofluorescent assays. Kaplan-Meier survival analysis and meta-analysis were used for survival analysis. GO(Gene-ontology) enrichment analysis, co-expression analysis, KEGG(Kyoto Encyclopedia of Genes and Genomes) pathway analysis, and immune infiltration analysis were performed to explore roles and related mechanisms of B2M in glioma., Results: We found that both B2M mRNA and protein levels were abnormally upregulated in glioma samples compared with those from normal brain tissue. B2M expression was correlated with tumor grade and was downregulated in IDH1 mutant samples. Furthermore, B2M was a moderately sensitive indicator for predicting the mesenchymal molecular subtype of gliomas. Interestingly, glioma patients with lower B2M expression had remarkably longer survival times than those with higher B2M expression. Moreover, meta-analysis showed that B2M was an independent predictive marker in glioma patients. The results of GO enrichment analysis revealed that B2M contributed to immune cell infiltration in glioma patients. In addition, results of KEGG pathway analysis and co-expression analysis suggested that B2M may mediate glioma immune infiltration via chemokines., Conclusions: We conclude that B2M levels are critical for the survival times of glioma patients, at least in part due to mediating high immune infiltration., (© 2021 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd.)

Inner Mongolia Cashmere goat is a well-known local cashmere goat breed in China. It is famous for excellent fleece quality and a significant advantage in cashmere yield compared to other cashmere goat breeds. In this study, a genome-wide association study was used to investigate fiber length, fiber diameter, and cashmere yield of 192 Inner Mongolia Cashmere goats using the Illumina GoatSNP52K Beadchip panel. We discovered that four single nucleotide polymorphisms (SNPs) reached genome-wide significance levels. These SNPs were located in some genes, e.g. FGF12, SEMA3D, EVPL, and SOX5, possibly related to fleece traits in Inner Mongolia Cashmere goat. Gene ontology enrichment analysis revealed that these genes were enriched in several biological pathways that were involved in hair follicle development in cashmere goats. In summary, the identified significant SNPs and genes provide useful information to explore genetic mechanisms underlying the variation in fleece traits and genomic selection of Chinese cashmere goat., (© 2021 The Authors. Animal Genetics published by John Wiley & Sons Ltd on behalf of Stichting International Foundation for Animal Genetics.)

The remodelling of structural and functional neurovascular unit (NVU) becomes a central therapeutic strategy after cerebral ischaemic stroke. In the present study, we investigated the effect of combined therapy of sodium ferulate (SF), n-butylidenephthalide (BP) and adipose-derived stromal cells (ADSCs) to ameliorate the injured NVU in the photochemically induced thrombotic stroke in rats. After solely or combined treatment, the neovascularization, activation of astrocytes, neurogenesis, expressions of vascular endothelial growth factor (VEGF) and claudin-5 were assessed by immunohistochemical or immunofluorescence staining. In order to uncover the underlying mechanism of therapeutic effect, signalling of protein kinase B/mammalian target of rapamycin (AKT/mTOR), extracellular signal-regulated kinase 1/2 (ERK1/2), and Notch1 in infarct zone were analysed by western blot. 18 F-2-deoxy-glucose/positron emission tomography, magnetic resonance imaging, Evans blue staining were employed to evaluate the glucose metabolism, cerebral blood flow (CBF), and brain-blood barrier (BBB) permeability, respectively. The results showed that combined treatment increased the neovascularization, neurogenesis, and VEGF secretion, modulated the astrocyte activation, enhanced the regional CBF, and glucose metabolism, as well as reduced BBB permeability and promoted claudin-5 expression, indicating the restoration of structure and function of NVU. The activation of ERK1/2 and Notch1 pathways and inhibition of AKT/mTOR pathway might be involved in the therapeutic mechanism. In summary, we have demonstrated that combined ADSCs with SF and BP, targeting the NVU remodelling, is a potential treatment for ischaemic stroke. These results may provide valuable information for developing future combined cellular and pharmacological therapeutic strategy for ischaemic stroke., (© 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

Aims: To investigate the safety of fluoxetine use during pregnancy, and to better understand the relationship between maternal fluoxetine use during the first trimester and congenital malformations in infants., Methods: PubMed and Web of Science databases were systematically searched from inception to 21 March 2016. Additional studies were identified in a manual search of the reference lists. Two reviewers independently extracted data. A third reviewer checked the data. Estimates were pooled using a random-effects model to calculate the summarized relative ratios (RR) and 95% confidence intervals (CI)., Results: Among 1918 initially identified articles, 16 cohort studies were included. The offspring of pregnant women exposed to fluoxetine during the first trimester had a statistically increased risk of major malformations (RR = 1.18, 95% CI = 1.08-1.29), cardiovascular malformations (RR = 1.36, 95% CI = 1.17-1.59), septal defects (RR = 1.38, 95% CI = 1.19-1.61), and non-septal defects (RR = 1.39, 95% CI = 1.12-1.73) with low heterogeneity in infants. There were no significant observations of other system-specific malformations in the nervous system, eye, urogenital system, digestive system, respiratory system, or musculoskeletal system, respectively. There was no indication of publication bias., Conclusions: The results of this meta-analysis indicate maternal fluoxetine use is associated with a slightly increased risk of cardiovascular malformations in infants. Health care providers and pregnant women must weigh the risk-benefit potential of these drugs when making decisions about whether to treat with fluoxetine during pregnancy., (© 2017 The British Pharmacological Society.)

New Findings: What is the central question of this study? High titres of autoantibodies against the second extracellular loop of the β 1 -adrenergic receptor (β 1 -AAs) can be detected in the sera of patients with ventricular arrhythmias, but a causal relationship between β 1 -AAs and ventricular arrhythmias has not been established. What is the main finding and its importance? Monoclonal β 1 -AAs (β 1 -AR mAbs) were used in the experiments. We showed that β 1 -AR mAbs increased susceptibility to ventricular arrhythmias and induced repolarization abnormalities. Antibody adsorption of β 1 -AAs will be a potential new therapeutic strategy for ventricular arrhythmias in patients with high titres of β 1 -AAs. High titres of autoantibodies against the second extracellular loop of the β 1 -adrenergic receptor (β 1 -AAs) can be detected in sera from patients with ventricular arrhythmias, but a causal relationship between β 1 -AAs and ventricular arrhythmias has not been established. In this work, ECGs of guinea-pigs and isolated guinea-pig hearts were recorded. Ventricular tachycardia (VT) and ventricular fibrillation (VF) were evoked by programmed electrical stimulation of the left ventricular epicardium of isolated guinea-pig hearts. The monophasic action potential and effective refractory period of the left ventricle were recorded in paced isolated guinea-pig hearts. Furthermore, to increase the specificity, monoclonal autoantibodies against the second extracellular loop of the β 1 -adrenergic receptor (β 1 -AR mAbs) were used in all experiments. The results showed that β 1 -AR mAbs induced premature ventricular contractions in guinea-pigs and isolated guinea-pig hearts. In addition, β 1 -AR mAbs decreased the threshold of VT/VF and prolonged the duration of VT/VF. Furthermore, β 1 -AR mAbs shortened the corrected QT interval and effective refractory period, and prolonged late-phase repolarization of the monophasic action potential (MAPD 90-30 ). These changes in electrophysiological parameters might be attributed, at least in part, to the arrhythmogenicity of β 1 -AR mAbs., (© 2016 The Authors. Experimental Physiology © 2016 The Physiological Society.)

In the title mol-ecule, C(7)H(4)N(2)O(2)S(2), the nitro group is twisted by 5.5 (1)° from the plane of the attached benzene ring. In the crystal, N-H⋯S hydrogen bonds link pairs of mol-ecules into inversion dimers, which are linked by weak C-H⋯O inter-actions into sheets parallel to (101). The crystal packing exhibits short inter-molecular S⋯O contacts of 3.054 (4) Å and π-π inter-actions of 3.588 (5) Å between the centroids of the five- and six-membered rings of neighbouring mol-ecules.

Endothelial progenitor cells (EPCs), which can be cultured in vitro from mononuclear cells in peripheral blood or bone marrow, express both hematopoietic stem cell and endothelial cell markers on their surface. They are believed to participate in endothelial repair and postnatal angiogenesis due to their abilities of differentiating into endothelial cells and secreting protective cytokines and growth factors. Mounting evidence suggests that circulating EPCs are reduced and dysfunctional in various diseases including hypertension, diabetes, coronary heart disease, and ischemic stroke. Therefore, EPCs have been documented to be a potential biomarker for vascular diseases and a hopeful candidate for regenerative medicine. Ischemic stroke, as the major cause of disability and death, still has limited therapeutics based on the approaches of vascular recanalization or neuronal protection. Emerging evidence indicates that transplantation of EPCs is beneficial for the recovery of ischemic cerebral injury. EPC-based therapy could open a new avenue for ischemic cerebrovascular disease. Currently, clinical trials for evaluating EPC transfusion in treating ischemic stroke are underway. In this review, we summarize the general conceptions and the characteristics of EPCs, and highlight the recent research developments on EPCs. More importantly, the rationale, perspectives, and strategies for using them to treat ischemic stroke will be discussed., (© 2012 Blackwell Publishing Ltd.)

Introduction: The delta opioid peptide [D-Ala2, D-Leu5]enkephalin (DADLE) plays a key role in neuronal protection against both hypoxic and ischemic conditions. However, the cellular mechanisms of action of DADLE under these conditions remain unclear., Methods: Ischemia was simulated with perfusing the brain slices with glucose-free artificial cerebrospinal fluid. Apoptosis was examined using an in situ cell death detection kit and expressed as the percentage of positively labeled neurons relative to total number of neurons. PCR was performed by adding cDNA, 5 pm dNTP, 1 μL Taqase, and primers. PCR products were separated with electrophoresis, stained with ethidium bromide, and visualized under ultraviolet light., Aims: To investigate the potential effects of DADLE in an ex vivo model of cerebral ischemia/reperfusion., Results: DADLE attenuated lactic dehydrogenase release and neuronal apoptosis in a concentration-dependent manner. The protective effects of DADLE were attenuated by representative selective delta2, but not delta1 opioid antagonists. Treatment with PD98059, a selective inhibitor of ERK kinase (MEK), also blocked the protective effect of DADLE as well as ERK phosphorylation induced by DADLE., Conclusions: Endogenous opioid peptides could promote cell survival via delta2 opioid receptors, possibly through the downstream MEK-ERK pathway., (© 2012 Blackwell Publishing Ltd.)

Objective: Fulminant hepatitis B is a clinical syndrome that results from massive necrosis of liver cells leading to the development of hepatic encephalopathy. The aim of this study was to evaluate the efficacy of lamivudine in patients with fulminant hepatitis B and study the prognostic factors., Methods: A matched retrospective cohort study using data on fulminant hepatitis B patients derived from our hospital database was conducted. Forty patients receiving lamivudine treatment were selected into the lamivudine treatment group with another 40 without lamivudine treatment studied as control. They were matched for sex, age and HBeAg status with lamivudine treatment group. The mortality of patients in two groups was compared. The influential factors on the mortality were studied by Cox proportional hazards model., Results: The mortality of patients in the lamivudine group (n=38) was significantly lower than that of the control group (n=39) (63.2 vs. 84.6%; χ(2) =4.609, P=0.032). For patients without systemic inflammatory response syndrome (SIRS), the mortality of patients in the lamivudine group (n=25) was significantly lower than that of the control group (n=26) (52.0 vs. 80.8%; χ(2) =4.747, P=0.029). In multivariate Cox proportional hazards analyses, for patients without SIRS, age (P=0.037), ratio of total to direct bilirubin (P=0.008), treatment method (P=0.005) and the decline of hepatitis B virus (HBV) DNA load during therapy (P=0.019) were independent predictors of prognosis., Conclusions: Treatment with lamivudine significantly decreases the mortality of fulminant hepatitis B patients without SIRS, and a rapid decline of HBV DNA load is one of the good predictors for the treatment outcome., (© 2011 John Wiley & Sons A/S.)

In the title compound, Na(2)CaNi(2)(P(2)O(7))(2)(H(2)O)(10), there are two distinct P-atom sites, each tetra-hedrally coordinated by four O atoms. The resulting phosphate tetra-hedra link through a common O atom, forming a [P(2)O(7)](4-) diphosphate unit. The Ni-O coordination is square pyramidal with four O atoms from two diphosphate groups in equatorial positions and the vertex occupied by a water O atom. The (P(2)O(7))(H(2)O) units link the Ni atoms, forming a chain of pyramids and tetra-hedra. As a result of the d-glide and twofold-axis symmetry of space group Fdd2, the chains propagate along [101] and [10], and chains in adjacent layers are mutually orthogonal. The Ca cation, located on a rotation axis, and the Na cation are each octa-hedrally coordinated by four O atoms and two waters. The Ni-chain arrangement is stabilized by Ca and Na coordination and a network of O-H⋯O hydrogen bonds.

The asymmetric unit of the title complex, [Zn(H(2)O)(6)](C(10)H(5)O(8))(2)·2C(11)H(6)N(2)O·2H(2)O, contains one half of the complex cation with the Zn(II) ion located on an inversion center, a monovalent 2,4,5-tricarboxybenzoate (1,2,4,5-BTC) counter-anion, a 4,5-diaza-fluoren-9-one (DAFO) mol-ecule and an uncoordinated water mol-ecule. In the crystal structure, O-H⋯O and O-H⋯N hydrogen bonds link the cations, anions and water mol-ecules into a three-dimensional network.

Objective: To study the virological features of patients coinfected with hepatitis B virus (HBV) and hepatitis C virus (HCV) and the efficacy of combination therapy with peginterferon alpha-2a and ribavirin in these patients., Methods: The epidemiological and virological data of 50 patients coinfected with HBV and HCV were analysed. The virological response rates of patients treated with peginterferon alpha-2a and ribavirin between the HBV and HCV coinfection group and the HCV monoinfection group were compared., Results: HCV-dominant virus strains accounted for 92.0% of the 50 coinfected individuals, and HCV- and HBV-dominant virus strains accounted for the remaining 8.0%. The HBV DNA level of the patients coinfected with HBV and HCV was 4.6+/-0.9 log(10) copies/ml, which was significantly lower than that in the HBV monoinfection group (5.9+/-1.2 log(10) copies/ml) (t=5.964, P<0.01). The HBeAg-positive rate (12.0%, 6/50) of the coinfection group was significantly lower than (45.3%, 19/42) that of the HBV monoinfection group (chi(2)=12.743, P<0.01). The partial early virological response (pEVR) rate and the end-of-treatment virological response (ETVR) rate (50.0%, 15/30; 90.0%, 27/30) of patients with genotype 1 in the coinfection group were significantly higher than those (16.0%, 4/25; 56.0%, 14/25) in the HCV monoinfection group (chi(2)=6.971, P=0.008; chi(2)=8.307, P=0.004). The relapse rate (55.6%, 15/27) of patients with genotype 1 in the coinfection group was significantly higher than that (21.4%, 3/14) in the HCV monoinfection group (chi(2)=4.360, P=0.037). The sustained virological response (SVR) rate (40.0%, 12/30) of patients with genotype 1 in the coinfection group was compared with that of the HCV monoinfection group (44.0%, 11/25) (chi(2)=0.090, P=0.765). There was no significant difference in the on-treatment virological response, ETVR, SVR and relapse rates between two groups for patients with genotype 2. The incidence of side effects (30%, 15/50) of patients in the coinfection group was significantly higher than that (13%, 6/46) in the HCV monoinfection group (chi(2)=4.031, P=0.045). The reactivation rate of HBV DNA (33.3%, 9/27) with HCV SVR was significantly higher than that of patients without SVR (8.7%, 2/23) (chi(2)=4.393, P=0.036)., Conclusions: The replication of HBV was suppressed, and HCV was the dominant virus strain. Compared with HCV-monoinfected patients, pEVR, ETVR and relapse rates of patients with genotype 1 in the coinfection group were high, while they shared similar SVR rates. HBV and HCV coinfection had no impact on the rate of virological response for genotype 2.

The title compound, [Cd(C(11)H(5)N(2)O(2))(2)(H(2)O)(2)], is a mononuclear complex consisting of a Cd(II) atom, two 3-hydr-oxy-4,5-diaza-fluoren-9-one ligands and two coordinated water mol-ecules. The Cd(II) atom, lying on a twofold axis, displays a distorted octa-hedral coordintion. Adjacent mol-ecules are linked by O-H⋯O hydrogen bonds and π-π inter-actions [centroid-centroid distance = 3.84 (1) Å], leading to a one-dimensional chain. Weak C-H⋯O hydrogen bonds connect the chains into a two-dimensional supra-molecular structure.

The novel title Zn(II) coordination polymer, poly[bis(mu-6-thioxo-1,6-dihydropyridine-3-carboxylato-kappa(2)S:O)zinc(II)], [Zn(C6H4NO2S)2]n, consists of two crystallographically independent zinc centers and two 6-mercaptonicotinate (Hmna-) ligands. Each Zn(II) atom is four-coordinated and lies at the center of a distorted tetrahedral ZnS2O2 coordination polyhedron, bridged by four Hmna- ligands to form a two-dimensional (4,4)-network. Each Hmna- ion acts as a bridging bidentate ligand, coordinating to two Zn(II) atoms through the S atom and a carboxyl O atom. The metal centers reside on twofold rotation axes. The coordination mode of the S atoms and N-H...O hydrogen-bonding interactions between the protonated N atoms and the uncoordinated carboxyl O atoms give the extended structure a wavelike form.

PbZn2(BO3)2 crystallizes in the space group Pccn, with the Pb cation at a site with imposed twofold symmetry. The compound represents a new structure type in which ZnBO3 layers are bridged by Pb2+ cations, giving rise to a three-dimensional framework. Channels parallel to the [010] direction accommodate the stereochemically active lone pairs of the Pb2+ cations.

A novel cadmium(II) coordination polymer, poly[[[bis(4,4'-bipyridine)cadmium(II)]-mu(3)-4,4'-dicarboxybiphenyl-3,3'-dicarboxylato] 0.35-hydrate], {[Cd(C(16)H(8)O(8))(C(10)H(8)N(2))(2)].0.35H(2)O}(n), was obtained by reaction of Cd(CH(3)COO)(2).3H(2)O, 4,4'-bipyridine (4,4'-bpy) and biphenyl-3,3',4,4'-tetracarboxylic acid (H(4)L) under hydrothermal conditions. Each Cd(II) atom lies at the centre of a distorted octahedron, coordinated by four O atoms from three H(2)L(2-) ligands and N atoms from two monodentate 4,4'-bpy ligands. Each H(2)L(2-) ligand coordinates to three Cd(II) atoms through two carboxylate groups, one acting as a bridging bidentate ligand and the other in a chelating bidentate fashion. Two Cd atoms, two H(2)L(2-) anions and four 4,4'-bpy ligands form a ring dimer node, which links into an extended broad zonal one-dimensional chain along the c axis.

Background: It was proved that higher haematocrit (Hct) might improve the function of brain after hypothermia circulation arrest (HCA). In the present study we established a new rat HCA model and investigated whether retrograde cerebral perfusion of oxygenated, compacted red blood cells (RBC) could attenuate brain injury after HCA., Methods: A new rat HCA model was developed and rats were randomly distributed into three groups: HCA group, HCA combined with retrograde cerebral perfusion of oxygenated, compacted red blood cell group (HCArcp group), and sham operation group (sham op. group). Animals both in the HCA group and in the HCArcp group underwent HCA 90 min at 18 degrees C. Brain damage after HCA was evaluated with light microscopy and electron microscopy. Immunohistochemistry and RT-PCR techniques were used to measured the different expressions of the C-Fos, Bcl-2, Bax mRNA and protein among the groups. Additionally we measured the wet/dry ratio of the brain in order to evaluate the oedema degree after HCA., Results: The new HCA model of rat we developed was comparable to the clinical setting not only in terms of the intubation, anaesthesia method and materials employed but also in terms of the priming volume in relation to body weight. The number of injured neurones in the hippocampus CA1 and parietal cortex, but not in the thalamus of the HCA group, was significantly greater than that of the HCArcp group (P<0.05). The mean score of mitochondrion of the hippocampus CA1 in the HCA group was significantly higher than in the HCArcp group (P<0.05). The expression of C-Fos, Bax mRNA and protein in the hippocampus CA1 and/or parietal cortex area was higher in the HCA group than in the HCArcp group (P<0.05). Expression of the mRNA and protein of Bcl-2 was higher in the HCArcp group than in the HCA group (P<0.05). The degree of oedema after HCA between the HCA group and HCArcp group had no significant difference (P>0.05)., Conclusions: We established a new rat model of HCA comparable to the clinical setting. Retrograde cerebral perfusion of oxygenated, compacted RBC is a simple, effective, and safe method to protect the brain during HCA. Adjusting the gene expression in relation to apoptosis might contribute to the neuroprotective effects of a retrograde cerebral infusion of oxygenated, compacted RBC.