Evaluation of Binding and Neutralizing Antibodies for Inactivated SARS-CoV-2 Vaccine Immunization.

The circulating severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) variant presents an ongoing challenge for surveillance and detection. It is important to establish an assay for SARS-CoV-2 antibodies in vaccinated individuals. Numerous studies have demonstrated that binding antibodies (such as S-IgG and N-IgG) and neutralizing antibodies (Nabs) can be detected in vaccinated individuals. However, it is still unclear how to evaluate the consistency and correlation between binding antibodies and Nabs induced by inactivated SARS-CoV-2 vaccines. In this study, serum samples from humans, rhesus macaques, and hamsters immunized with inactivated SARS-CoV-2 vaccines were analyzed for S-IgG, N-IgG, and Nabs. The results showed that the titer and seroconversion rate of S-IgG were significantly higher than those of N-IgG. The correlation between S-IgG and Nabs was higher compared to that of N-IgG. Based on this analysis, we further investigated the titer thresholds of S-IgG and N-IgG in predicting the seroconversion of Nabs. According to the threshold, we can quickly determine the positive and negative effects of the SARS-CoV-2 variant neutralizing antibody in individuals. These findings suggest that the S-IgG antibody is a better supplement to and confirmation of SARS-CoV-2 vaccine immunization.

The mechanisms of mitochondrial abnormalities that contribute to sleep disorders and related neurodegenerative diseases.

Sleep is a highly intricate biological phenomenon, and its disorders play a pivotal role in numerous diseases. However, the specific regulatory mechanisms remain elusive. In recent years, the role of mitochondria in sleep disorders has gained considerable attention. Sleep deprivation not only impairs mitochondrial morphology but also decreases the number of mitochondria and triggers mitochondrial dysfunction. Furthermore, mitochondrial dysfunction has been implicated in the onset and progression of various sleep disorder-related neurological diseases, especially neurodegenerative conditions. Therefore, a greater understanding of the impact of sleep disorders on mitochondrial dysfunction may reveal new therapeutic targets for neurodegenerative diseases. In this review, we comprehensively summarize the recent key findings on the mechanisms underlying mitochondrial dysfunction caused by sleep disorders and their role in initiating or exacerbating common neurodegenerative diseases. In addition, we provide fresh insights into the diagnosis and treatment of sleep disorder-related diseases.

Correction to "Research on the Optimization for Acidification Modification Scheme Considering Coal's Wettability Based on the AHP-TOPSIS Method".

[This corrects the article DOI: 10.1021/acsomega.3c03428.].

Enhancing Electrochemical Signal for Efficient Chiral Recognition by Encapsulating C60 Fullerene into Chiral Lanthanum-Based MOFs.

Chiral metal-organic frameworks (MOFs) have attracted much attention due to their highly tunable regular microporous structures. However, chiral electrochemical recognition based on chiral MOFs is often limited by poor charge separation and slow charge transfer kinetics. In this case, C60 can be encapsulated into the cavity of [La(BTB)]n by virtue of host-guest interactions through π-π stacking to synthesize the chiral composite C60@[La(BTB)]n and amplify electrochemically controlled enantioselective interactions with the target enantiomers. A large electrostatic potential difference is generated in chiral C60@[La(BTB)]n due to the host-guest interaction and the inhomogeneity of the charge distribution, leading to the generation of a strong built-in electric field and thus an overall enhancement of the conductivity of the chiral material. Their enantioselective detection of tryptophan enantiomers was demonstrated by electrochemical measurement. The results showed that chiral MOF materials can be used for enantiomeric recognition. It is worth noting that this new material derived from the concept of host-guest interaction to enhance charge separation opens up unprecedented possibilities for future enantioselective recognition and separation.

Fabrication strategies for chiral self-assembly surface.

Chiral self-assembly is the spontaneous organization of individual building blocks from chiral (bio)molecules to macroscopic objects into ordered superstructures. Chiral self-assembly is ubiquitous in nature, such as DNA and proteins, which formed the foundation of biological structures. In addition to chiral (bio) molecules, chiral ordered superstructures constructed by self-assembly have also attracted much attention. Chiral self-assembly usually refers to the process of forming chiral aggregates in an ordered arrangement under various non-covalent bonding such as H-bond, π-π interactions, van der Waals forces (dipole-dipole, electrostatic effects, etc.), and hydrophobic interactions. Chiral assembly involves the spontaneous process, which followed the minimum energy rule. It is essentially an intermolecular interaction force. Self-assembled chiral materials based on chiral recognition in electrochemistry, chiral catalysis, optical sensing, chiral separation, etc. have a broad application potential with the research development of chiral materials in recent years.

Trifluoperazine regulates blood-brain barrier permeability via the MLCK/p-MLC pathway to promote ischemic stroke recovery.

Blood-brain barrier (BBB) disruption following ischemic stroke (IS) can induce significant aftereffects. Elevated calmodulin (CaM) expression following stroke causes calcium overload-a key contributor to BBB collapse. Trifluoperazine (TFP), a CaM inhibitor, reduces CaM overexpression following IS. However, it remains unclear whether TFP participates in BBB repair after IS. We administered TFP to mice subjected to middle cerebral artery occlusion (MCAO) and bEnd.3 cells subjected to oxygen-glucose deprivation (OGD). TFP treatment in MCAO mice reduced cerebral CaM expression and infarct size and decreased BBB permeability. OGD-treated bEnd.3 cells showed significantly increased CaM protein levels and reduced tight junction (TJ) protein levels; these changes were reversed by TFP treatment. Our results found that TFP administration in mice inhibited actin contraction following cerebral ischemia-reperfusion by suppressing the MLCK/p-MLC pathway, thereby attenuating cell retraction, improving TJ protein integrity, and reducing BBB permeability. Consequently, this treatment may promote neurological function recovery after IS.

Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K-AKT pathway by bioinformatic analysis.

Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-two SD rats were randomly divided into three groups: middle cerebral artery occlusion (MCAO) group, exercise group with MCAO (EX + MCAO) group, and sham group, with 14 rats in each group. The EX + MCAO group underwent exercise preconditioning for 3 weeks before occlusion, and the other two groups were fed and exercised normally. After 3 weeks, MCAO model was made by thread plug method in the EX + MCAO group and MCAO group. After successful modeling, the Longa scale was used to evaluate the neurological impairment of rats at day 0, day 1, and day 2. The rats in each group were killed on the third day after modeling. TTC staining measured the infarct volume of each group. The morphology and apoptosis of cortical cells were observed by HE and Tunel staining. Three rats in each group underwent high-throughput sequencing. Bioinformatic analysis was used to find the deferentially expressed genes (DEGs) and predict the transcription factor binding sites (TFBS) of the next-generation sequencing results. Gene enrichment (GSEA) was used to analyze potential functional genes and their corresponding signaling pathways. The Longa scale showed EX + MCAO group had the neurological function better than the modeling group (P < 0.001). TTC staining showed that the infarct size of EX + MCAO group was less than MCAO group (P < 0.05). HE and Tunel staining showed that the cells in the EX + MCAO group and the sham group had normal morphology and fewer apoptotic cells than MCAO group. A new gene named 7994 was discovered and TFBS of this gene was predicted, which could interact with key genes such as Foxd3, Foxa2, NR4A2, SP1, CEBPA, and SOX10. GSEA showed that EX + MCAO group could promote and regulate angiogenesis and apoptosis through PI3K-AKT pathway. Preconditioning exercise could improve nerve function and reduce infarct size in rats. The underlying mechanism is to regulate the PI3K-AKT pathway through several key genes, promote cerebral angiogenesis, and reduce apoptosis.

Spine plasticity of dentate gyrus parvalbumin-positive interneurons is regulated by experience.

Experience-driven alterations in neuronal activity are followed by structural-functional modifications allowing cells to adapt to these activity changes. Structural plasticity has been observed for cortical principal cells. However, how GABAergic interneurons respond to experience-dependent network activity changes is not well understood. We show that parvalbumin-expressing interneurons (PVIs) of the dentate gyrus (DG) possess dendritic spines, which undergo behaviorally induced structural dynamics. Glutamatergic inputs at PVI spines evoke signals with high spatial compartmentalization defined by neck length. Mice experiencing novel contexts form more PVI spines with elongated necks and exhibit enhanced network and PVI activity and cFOS expression. Enhanced green fluorescent protein reconstitution across synaptic partner-mediated synapse labeling shows that experience-driven PVI spine growth boosts targeting of PVI spines over shafts by glutamatergic synapses. Our findings propose a role for PVI spine dynamics in regulating PVI excitation by their inputs, which may allow PVIs to dynamically adjust their functional integration in the DG microcircuitry in relation to network computational demands.

Hierarchical classification of early microscopic lung nodule based on cascade network.

Purpose: Early-stage lung cancer is typically characterized clinically by the presence of isolated lung nodules. Thousands of cases are examined each year, and one case usually contains numerous lung CT slices. Detecting and classifying early microscopic lung nodules is demanding due to their diminutive dimensions and restricted characterization capabilities. Therefore, a lung nodule classification model that performs well and is sensitive to microscopic lung nodules is needed to accurately classify lung nodules. Methods: This paper uses the Resnet34 network as a basic classification model. A new cascade lung nodule classification method is proposed to classify lung nodules into 6 classes instead of the traditional 2 or 4 classes. It can effectively classify six different nodule types including ground-glass and solid nodules, benign and malignant nodules, and nodules with predominantly ground-glass or solid components. Results: In this paper, the traditional multi-classification method and the cascade classification method proposed in this paper were tested using real lung nodule data collected in the clinic. The test results demonstrate that the cascade classification method in this study achieves an accuracy of 80.04%, outperforming the conventional multi-classification approach. Conclusions: Different from the existing methods for categorizing the benign and malignant nature of lung nodules, the approach presented in this paper can classify lung nodules into 6 categories more accurately. At the same time, This paper proposes a rapid, precise, and dependable approach for classifying six distinct categories of lung nodules, which increases the accuracy categorization compared with the traditional multivariate categorization method.

pH-Tuned Enantioselectivity Reversal in a Defective Chiral Metal Organic Framework.

The introduction of chirality into easy-scalable metal-organic frameworks (MOFs) gives rise to the development of advanced electrochemical sensors. However, integrating chirality by directly connecting metal ions and chiral ligands is unpredictable. Postmodification synthesis is a common method for synthesizing chiral MOFs, but it reduces the size of chiral channels and poses obstacles to the approach of chiral guest molecules. In this work, missing connection defects were introduced into the chiral MOFs through defect engineering strategies, which enhance the recognition of the target enantiomers. pH can tune enantioselectivity reversal in defective chiral MOFs. The chiral MOFs show enantioselectivity for d-Trp at pH = 5 and l-Trp at pH = 8. From the results of zeta potential, regardless of pH 5 or 8, the chiral MOF has a positive potential. The chiral MOFs are positively charged, while tryptophan is negatively charged when pH = 8. The difference in the positive and negative charge interactions between the two amino acids and chiral MOFs leads to chiral recognition. However, the difference in π-π interaction between chiral MOF and Trp enantiomers mainly drives chiral recognition under pH = 5. This study paves a pathway for the synthesis of defective chiral MOFs and highlights the pH-tuned enantioselectivity reversal.

A novel nomogram predicting early neurological deterioration after intravenous thrombolysis for acute ischemic stroke.

Objectives: Intravenous thrombolysis therapy (IVT) with recombinant tissue plasminogen activator has proven to be a beneficial treatment for acute ischemic stroke (AIS) patients when administered within 4.5 h after a stroke. This study aimed to investigate an available and inexpensive predictive tool for early neurological deterioration in AIS. Methods: Patients admitted to our department with acute stroke who were given IVT with recombinant tissue plasminogen activator within 4.5 h of stroke onset were included in the study. The NIH stroke scale (NIHSS) was used to assess patients' neurological state prior to IVT and for 24 h after. Early neurological deterioration was defined as occurring if the NIHSS total score increased by ≥ 4 or the NIHSS individual score increased by ≥ 2 compared to baseline. Patients were randomly assigned to training or validation cohorts. Results: Of the 266 AIS patients receiving IVT who were screened, 217 were deemed eligible for the study. Multivariate logistic regression analysis identified smoking history, NIHSS score, homocysteine level, and neutrophil to lymphocyte ratio as independent factors for predicting early neurological deterioration. ROC analysis was used to assess the quality of the resulting nomogram. The AUC for the training dataset was 0.826 (95 % CI, 0.719-0.932), and for the validation dataset was 0.887 (95 % CI, 0.763-1.000). Conclusion: The robustness of this nomogram suggests that it may be a reliable tool for evaluating the progression of AIS after IVT.

Latent class analysis of the sleep quality of night shift nurses and impact of shift-related factors on the occupational stress and anxiety.

AIMS: The objective of this study is to explore the various latent categories within the sleep quality of night shift nurses and to investigate whether shift-related factors predispose nurses to higher levels of occupational stress and anxiety. DESIGN: This is a cross-sectional study. METHODS: From November to December 2020, registered nurses from 18 tertiary hospitals and 16 secondary hospitals in Chongqing were selected through convenience sampling for this study. Latent class analysis was used to investigate the sleep quality of nurses working night shifts. Furthermore, univariate analysis and logistic multivariate analysis were utilized to identify the contributing factors to occupational stress and anxiety. RESULTS: The four latent categories of Pittsburgh Sleep Quality Index for night shift nurses were identified as 'Low Sleep Disorder Group' (56.34%), 'Moderate Sleep Disorder Group' (37.27%), 'High Sleep Disorder Non-Reliant on Sleeping medication Group' (4.89%) and 'High Sleep Disorder Reliant on Sleeping medication Group' (1.50%). The results showed that having a night-shift frequency of 3-4 times per month, night-shift durations of 9-12 h, sleep time delay after night shift (≥2 h), total sleep time after night shift less than 4 h were shift-related factors that increased the levels of occupational stress and anxiety. CONCLUSION: The sleep quality of night shift nurses demonstrates heterogeneity and can be classified into four latent categories. Higher frequency of night shifts, extended work hours and insufficient rest time are all associated with increased levels of occupational stress and anxiety. IMPACT: By identifying the four latent categories of sleep quality among night shift nurses, this study sheds light on the relationship between sleep patterns and levels of occupational stress and anxiety. These findings have important implications for healthcare institutions in the management of nurse well-being and work schedules. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution.

Two-component system LiaSR negatively regulated the acid resistance and pathogenicity of Listeria monocytogenes 10403S.

The glutamate decarboxylase (GAD) system is one of the acid-resistant systems of Listeria monocytogenes (L. monocytogenes), while the regulatory mechanism of GadT2/GadD2, which plays the major role in the GAD system for acid resistance, is not clear. The two-component system (TCS) is a signal transduction system that is also involved in regulating acid resistance in bacteria. By screening the TCSs of L. monocytogenes 10403S, we found that knocking out the TCS LisSR (encoded by lmo1021/lmo1022) led to a significant increase in the transcription and expression of the gadT2/gadD2 cluster. Subsequently, we constructed a complemental strain CΔliaSR. and a complemental strain with LiaS His157 to Ala, which was designated as CΔliaSRH157A. Survival assay, transcriptional and expression analysis and pathogenicity assay revealed that liaSR deletion significantly enhanced the acid resistance and pathogenicity of 10403S and significantly increased the gadT2/gadD2 transcription and expression. Mutating LiaS His157 to Ala significantly enhanced the acid resistance and pathogenicity of CΔliaSR and significantly increased the gadT2/gadD2 transcription and expression. The results suggest that the two-component system LiaSR mediates the acid resistance and pathogenicity in 10403S by inhibiting the gadT2/gadD2 cluster, and the key activation site of LiaS is His157. This study provides novel knowledge on the regulation of GAD system and the control of this foodborne pathogen.

Deregulation of the Glymphatic System in Alzheimer's Disease: Genetic and Non-Genetic Factors.

Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by progressive degeneration of brain function. AD gradually affects the parts of the brain that control thoughts, language, behavior and mental function, severely impacting a person's ability to carry out daily activities and ultimately leading to death. The accumulation of extracellular amyloid-ß peptide (Aß) and the aggregation of intracellular hyperphosphorylated tau are the two key pathological hallmarks of AD. AD is a complex condition that involves both non-genetic risk factors (35%) and genetic risk factors (58-79%). The glymphatic system plays an essential role in clearing metabolic waste, transporting tissue fluid, and participating in the immune response. Both non-genetic and genetic risk factors affect the glymphatic system to varying degrees. The main purpose of this review is to summarize the underlying mechanisms involved in the deregulation of the glymphatic system during the progression of AD, especially concerning the diverse contributions of non-genetic and genetic risk factors. In the future, new targets and interventions that modulate these interrelated mechanisms will be beneficial for the prevention and treatment of AD.

Predicting visceral pleural invasion in lung adenocarcinoma presenting as part-solid density utilizing a nomogram model combined with radiomics and clinical features.

BACKGROUND: To develop and validate a preoperative nomogram model combining the radiomics signature and clinical features for preoperative prediction of visceral pleural invasion (VPI) in lung nodules presenting as part-solid density. METHODS: We retrospectively reviewed 156 patients with pathologically confirmed invasive lung adenocarcinomas after surgery from January 2016 to August 2019. The patients were split into training and validation sets by a ratio of 7:3. The radiomic features were extracted with the aid of FeAture Explorer Pro (FAE). A CT-based radiomics model was constructed to predict the presence of VPI and internally validated. Multivariable regression analysis was conducted to construct a nomogram model, and the performance of the models were evaluated with the area under the receiver operating characteristic curve (AUC) and compared with each other. RESULTS: The enrolled patients were split into training (n = 109) and validation sets (n = 47). A total of 806 features were extracted and the selected 10 optimal features were used in the construction of the radiomics model among the 707 stable features. The AUC of the nomogram model was 0.888 (95% CI: 0.762-0.961), which was superior to the clinical model (0.787, 95% CI: 0.643-0.893; p = 0.049) and comparable to the radiomics model (0.879, 95% CI: 0.751-0.965; p > 0.05). The nomogram model achieved a sensitivity of 90.5% and a specificity of 76.9% in the validation dataset. CONCLUSIONS: The nomogram model could be considered as a noninvasive method to predict VPI with either highly sensitive or highly specific diagnoses depending on clinical needs.

Neuroprotective effect of the traditional decoction Tian-Si-Yin against Alzheimer's disease via suppression of neuroinflammation.

ETHNOPHARMACOLOGICAL RELEVANCE: Alzheimer's disease (AD) is the most prevalent neurodegenerative disease among old adults. As a traditional Chinese medicine, the herbal decoction Tian-Si-Yin consists of Morinda officinalis How. and Cuscuta chinensis Lam., which has been widely used to nourish kidney. Interestingly, Tian-Si-Yin has also been used to treat dementia, depression and other neurological conditions. However, its therapeutic potential for neurodegenerative diseases such as AD and the underlying mechanisms remain unclear. AIM OF THE STUDY: To evaluate the therapeutic effect of the herbal formula Tian-Si-Yin against AD and to explore the underlying mechanisms. MATERIALS AND METHODS: The N2a cells treated with amyloid ß (Aß) peptide or overexpressing amyloid precursor protein (APP) were used to establish cellular models of AD. The in vivo anti-AD effects were evaluated by using Caenorhabditis elegans and 3 × Tg-AD mouse models. Tian-Si-Yin was orally administered to the mice for 8 weeks at a dose of 10, 15 or 20 mg/kg/day, respectively. Its protective role on memory deficits of mice was examined using the Morris water maze and fear conditioning tests. Network pharmacology, proteomic analysis and ultra-high performance liquid chromatography-mass spectrometry/mass spectrometry (UHPLC-MS/MS) were used to explore the underlying molecular mechanisms, which were further investigated by Western blotting and immunohistochemistry. RESULTS: Tian-Si-Yin was shown to improve cell viability of Aß-treated N2a cells and APP-expressing N2a-APP cells. Tian-Si-Yin was also found to reduce ROS level and extend lifespan of transgenic AD-like C. elegans model. Oral administration of Tian-Si-Yin at medium dose was able to effectively rescue memory impairment in 3 × Tg mice. Tian-Si-Yin was further shown to suppress neuroinflammation by inhibition of glia cell activation and downregulation of inflammatory cytokines, diminishing tau phosphoralytion and Aß deposition in the mice. Using UHPLC-MS/MS and network pharmacology technologies, 17 phytochemicals from 68 components of Tian-Si-Yin were identified as potential anti-AD components. MAPK1, BRAF, TTR and Fyn were identified as anti-AD targets of Tian-Si-Yin from network pharmacology and mass spectrum. CONCLUSIONS: This study has established the protective effect of Tian-Si-Yin against AD and demonstrates that Tian-Si-Yin is capable of improving Aß level, tau pathology and synaptic disorder by regulating inflammatory response.

Association between MC1R gene and coat color segregation in Shanxia long black pig and Lulai black pig.

BACKGROUND: Coat color, as a distinct phenotypic characteristic of pigs, is often subject to preference and selection, such as in the breeding process of new breed. Shanxia long black pig was derived from an intercross between Berkshire boars and Licha black pig sows, and it was bred as a paternal strain with high-quality meat and black coat color. Although the coat color was black in the F1 generation of the intercross, it segregated in the subsequent generations. This study aims to decode the genetic basis of coat color segregation and develop a method to distinct black pigs from the spotted in Shanxia long black pig. RESULTS: Only a QTL was mapped at the proximal end of chromosome 6, and MC1R gene was picked out as functional candidate gene. A total of 11 polymorphic loci were identified in MC1R gene, and only the c.67_68insCC variant was co-segregating with coat color. This locus isn't recognized by any restriction endonuclease, so it can't be genotyped by PCR-RFLP. The c.370G > A polymorphic locus was also significantly associated with coat color, and has been in tightly linkage disequilibrium with the c.67_68insCC. Furthermore, it is recognized by BspHI. Therefore, a PCR-RFLP method was set up to genotype this locus. Besides the 175 sequenced individuals, another more 1,391 pigs were genotyped with PCR-RFLP, and all of pigs with GG (one band) were black. CONCLUSION: MC1R gene (c.67_68insCC) is the causative gene (mutation) for the coat color segregation, and the PCR-RFLP of c.370G > A could be used in the breeding program of Shanxia long black pig.

Impact of Personal Protective Equipment on Cardiopulmonary Resuscitation and Rescuer Safety.

Background: High-quality cardiopulmonary resuscitation (CPR) is a key element in the rescue of cardiac arrest patients but is difficult to achieve in circumstances involving aerosol transmission, such as the COVID-19 pandemic. Methods: This prospective randomized crossover trial included 30 experienced health care providers to evaluate the impact of personal protective equipment (PPE) on CPR quality and rescuer safety. Participants were asked to perform continuous CPR for 5 minutes on a manikin with three types of PPE: level D-PPE, level C-PPE, and PAPR. The primary outcome was effective chest compression per minute. Secondary outcomes were the fit factor by PortaCount, vital signs and fatigue scores before and after CPR, and perceptions related to wearing PPE. Repeated-measures ANOVA was used, and a two-tailed test value of 0.05 was considered statistically significant. Results: The rates of effective chest compressions for 5 minutes with level D-PPE, level C-PPE, and PAPRs were 82.0 ± 0.2%, 78.4 ± 0.2%, and 78.0 ± 0.2%, respectively (p = 0.584). The fit-factor test values of level C-PPE and PAPRs were 182.9 ± 39.9 vs. 198.9 ± 9.2 (p < 0.001). The differences in vital signs before and after CPR were not significantly different among the groups. In addition, the fatigue and total perception scores of wearing PPE were significantly higher for level C-PPE than PAPRs: 3.8 ± 1.6 vs. 3.0 ± 1.6 (p < 0.001) and 27.9 ± 5.4 vs. 26.0 ± 5.3 (p < 0.001), respectively. Conclusion: PAPRs are recommended when performing CPR in situations where aerosol transmission is suspected. When PAPRs are in short supply, individual fit-tested N95 masks are an alternative. This trial is registered with NCT04802109.

[Muscone inhibits opening of mPTP to alleviate OGD/R-induced injury of HT22 cells].

This study aims to investigate the mechanism of muscone in inhibiting the opening of mitochondrial permeability transition pore(mPTP) to alleviate the oxygen and glucose deprivation/reoxygenation(OGD/R)-induced injury of mouse hippocampal neurons(HT22). An in vitro model of HT22 cells injured by OGD/R was established. CCK-8 assay was employed to examine the viability of HT22 cells, fluorescence microscopy to measure the mitochondrial membrane potential, the content of reactive oxygen species(ROS), and the opening of mPTP in HT22 cells. Enzyme-linked immunosorbent assay was employed to determine the level of ATP and the content of cytochrome C(Cyt C) in mitochondria of HT22 cells. Flow cytometry was employed to determine the Ca~(2+) content and apoptosis of HT22 cells. The expression of Bcl-2(B-cell lymphoma-2) and Bcl-2-associated X protein(Bax) was measured by Western blot. Molecular docking and Western blot were employed to examine the binding between muscone and methyl ethyl ketone(MEK) after pronase hydrolysis of HT22 cell proteins. After the HT22 cells were treated with U0126, an inhibitor of MEK, the expression levels of MEK, p-ERK, and CypD were measured by Western blot. The results showed that compared with the OGD/R model group, muscone significantly increased the viability, mitochondrial ATP activity, and mitochondrial membrane potential, lowered the levels of ROS, Cyt C, and Ca~(2+), and reduced mPTP opening to inhibit the apoptosis of HT22 cells. In addition, muscone up-regulated the expression of MEK, p-ERK, and down-regulated that of CypD. Molecular docking showed strong binding activity between muscone and MEK. In conclusion, muscone inhibits the opening of mPTP to inhibit apoptosis, thus exerting a protective effect on OGD/R-injured HT22 cells, which is associated with the activation of MEK/ERK/CypD signaling pathway.