CELLULAR AND MOLECULAR BIOLOGY细胞与分子生物学
CELLULAR AND MOLECULAR BIOLOGY,ISSN 0145-5680,eISSN 1165-158X,中文译名:细胞与分子生物学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2020 | 1.770 | Q4 |
| 2021 | 1.206 | Q4 |
| 2022 | 1.600 | Q4 |
| 2023 | 1.500 | Q4 |
CELLULAR AND MOLECULAR BIOLOGY 最新收录文献
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1. Cognitive-enhancing effects of a herbal combination on D‑galactose‑induced memory impairment.
PMID:日期:2026-05-31Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss, for which effective pharmacological interventions remain limited. This study investigated the cognitive-enhancing effects of an optimized six‑herbal combination (HC) comprising Polygonati Rhizoma (PR), Lycium barbarum polysaccharides (LBPs), Green Tea (GT), Jujube Seeds (JS), Fructus hippophae (FH), and Mori Folium (MF). Using the Ellman method, we evaluated the acetylcholinesterase (AChE) inhibitory activities of individual herbs and HC. An L₂₅(4⁶) orthogonal design was employed to determine the optimal proportions of the six herbs, with AChE inhibition as the evaluation index. The optimal HC composition (PR 9 g, LBPs 6 g, GT 3 g, JS 3 g, FH 3 g, MF 5 g) exhibited 88.11% AChE inhibition at 2000 μg/mL, which was significantly higher than that of any individual herb (p < 0.05). Network pharmacology analysis revealed 682 common targets between HC and AD, with significant enrichment in the PI3K‑Akt signaling pathway, lipid metabolism, and chemical carcinogenesis‑receptor activation pathways, suggesting multi‑target mechanisms of action. In a D‑galactose‑induced subacute aging mouse model (3.5 g·kg⁻¹, 70 days), HC treatment (0.75, 1.5, and 3.0 g·kg⁻¹, 28 days) significantly improved spatial learning and memory in the Morris water maze. Specifically, HC at 1.5 g·kg⁻¹ significantly reduced escape latency (p < 0.01 vs. D‑galactose group), increased superoxide dismutase (SOD) and glutathione (GSH) levels (p < 0.05), and decreased malondialdehyde (MDA) and monoamine oxidase (MAO) levels (p < 0.01), while ameliorating hippocampal neuronal damage, as confirmed by hematoxylin and eosin staining. These findings demonstrate that HC exhibits potent anti‑cholinesterase activity, modulates oxidative stress, and protects against neuronal injury, positioning it as a promising multi‑target botanical candidate for further development in the prevention and management of AD.
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2. Chelidonium majus L. alkaloid extract encapsulated in human serum albumin nanoparticles induces mitochondria-mediated apoptosis in HeLa cell line.
PMID:日期:2026-05-31Interest in herbal medicines as complementary therapies has increased because of concerns regarding the adverse effects of conventional chemotherapeutic agents. Chelidonium majus L. (C. majus) exhibits antiproliferative activity against several cancer cell lines; however, its therapeutic efficacy may be limited by poor bioavailability. This study evaluated the apoptotic activity of C. majus alkaloid extract encapsulated in human serum albumin nanoparticles (C. majus/HSA-NPs) in HeLa cervical cancer cells. Cytotoxicity of C. majus alkaloid extract (C. majus/AE), C. majus/HSA-NPs, and HSA-NPs was determined using the MTT assay in HeLa and human fibroblast cells, apoptosis was quantified by Annexin V/PI flow cytometry, and the mRNA expression of Bax, Bcl-2, caspase-9 and caspase-3 was analyzed by real-time RT-PCR. After 48 h, the IC₅₀ values in HeLa cells were 70.79 μg/mL for C. majus/AE, 52.37 μg/mL for C. majus/HSA-NPs, and >2000 μg/mL for HSA-NPs, whereas fibroblast cells exhibited substantially higher IC₅₀ values (835 μg/mL for C. majus/AE and >1600 μg/mL for both C. majus/HSA-NPs and HSA-NPs), indicating selective cytotoxicity toward cancer cells. C. majus/HSA-NPs induced significantly greater apoptosis than the free alkaloid extract and markedly enhanced the expression of the pro-apoptotic genes Bax, caspase-9, and caspase-3, while suppressing Bcl-2, resulting in a significantly higher Bax/Bcl-2 ratio, consistent with activation of the mitochondrial apoptotic pathway. Overall, nanoencapsulation with human serum albumin enhanced the anticancer efficacy of C. majus alkaloids while maintaining low toxicity toward normal fibroblasts, suggesting that C. majus/HSA-NPs represent a promising candidate for targeted cervical cancer therapy, although further in vivo and mechanistic studies are required to confirm their therapeutic potential.
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3. Congruency of exosome-mediated blood-brain barrier dysfunction by activation of Na/K-ATPase in obstructive sleep apnea and Alzheimer's disease.
PMID:日期:2026-05-31Obstructive sleep apnea (OSA) and Alzheimer's disease (AD) are highly prevalent chronic disorders that share several pathological features, including oxidative stress, inflammation, vascular dysfunction, and cognitive impairment. Although epidemiological studies have demonstrated a strong association between OSA and an increased risk of AD, the mechanisms linking these disorders remain poorly understood. We hypothesized that circulating plasma exosomes from patients with OSA or AD disrupt blood-brain barrier (BBB) integrity through activation of Na⁺/K⁺-ATPase signaling. Plasma exosomes were isolated from adult male patients with OSA or AD (n = 10/group) and applied to naïve human brain microvascular endothelial cells (hCMEC/D3). BBB integrity was continuously monitored using electric cell-substrate impedance sensing (ECIS) in the presence or absence of the Na⁺/K⁺-ATPase signaling inhibitor pNaKtide (0-2.0 µM). Exosomes derived from both OSA and AD patients significantly impaired endothelial barrier function, indicating that circulating extracellular vesicles carry bioactive cargo capable of disrupting BBB integrity. Pharmacological inhibition of Na⁺/K⁺-ATPase signaling with pNaKtide significantly restored barrier function at concentrations of 1.0 and 2.0 µM, although the degree of protection differed between the OSA- and AD-derived exosomes, suggesting disease-specific mechanisms of endothelial injury. These findings identify Na⁺/K⁺-ATPase signaling as a key mediator of exosome-induced BBB dysfunction and provide mechanistic evidence linking circulating extracellular vesicles to neurovascular injury in both OSA and AD. Collectively, our results suggest that plasma-derived exosomes contribute to BBB disruption and highlight Na⁺/K⁺-ATPase signaling as a promising therapeutic target for preventing or attenuating neurovascular dysfunction associated with OSA and AD.
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4. Molecular epidemiology of antimicrobial-resistant Klebsiella pneumoniae in intensive care unit patients, southwestern Saudi Arabia.
PMID:日期:2026-05-31Antimicrobial resistance (AMR) in Gram-negative pathogens poses a critical threat in intensive care units (ICUs). This retrospective observational study aimed to determine the prevalence and phenotypic resistance profiles of extended-spectrum β‑lactamase (ESBL)-producing and carbapenem‑resistant Klebsiella pneumoniae among ICU patients at a tertiary hospital in southwestern Saudi Arabia (2020-2021). Clinical specimens (n=179) from patients with hospital‑acquired infections were processed using standard culture, Vitek 2 identification, and phenotypic confirmatory tests (combination disc test for ESBLs and modified carbapenem inactivation method for carbapenemase). Of 543 total samples, 49 (9.0%) were identified as K. pneumoniae. ESBL production was detected in 15/49 (30.6%) and carbapenemase production in 6/49 (12.2%) of isolates. The highest resistance rates were observed against piperacillin‑tazobactam (55.1%), cefotaxime (55.1%), imipenem (53.0%), and meropenem (53.0%), while tigecycline (100% susceptibility) and amikacin (93.9% susceptibility) remained the most effective agents. Notably, susceptibility to trimethoprim‑sulfamethoxazole was 83.7% (corrected figure). Children under 10 years and adults aged 21-40 years showed the highest infection rates. The alarmingly high prevalence of ESBL and carbapenemase phenotypes, coupled with significant multidrug resistance, underscores the urgent need for routine molecular surveillance and targeted antibiotic stewardship in this region. Rapid phenotypic screening combined with genotypic confirmation is essential to guide empirical therapy and curb the spread of these high‑risk clones in critically ill populations.
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5. Autotaxin as a potential biomarker in hepatic encephalopathy: Insights from a mouse model and cirrhotic patients.
PMID:日期:2026-05-31Hepatic encephalopathy (HE) is a debilitating neuropsychiatric condition associated with acute liver failure or advanced liver diseases, significantly affecting patient morbidity and mortality. Autotaxin (ATX), a lysophospholipase D that generates lysophosphatidic acid (LPA), has been proposed as a biomarker for liver fibrosis progression, but its role in HE remains poorly defined. This study aimed to explore the potential roles of ATX using in vivo TAA-induced HE models in mouse and clinical evaluations of cirrhotic patients with and without HE. ATX concentrations were quantified in plasma, liver tissue, and frontal cortex of HE mice, while ectonucleotide pyrophosphatase/phosphodiesterase 2 (Enpp2) gene expression and LPA levels were assessed in murine salivary glands. In parallel, serum and salivary ATX were measured in 7 cirrhotic patients with HE and 12 cirrhotic patients without HE. ATX concentrations were significantly elevated in the liver parenchyma and frontal cortex of TAA-induced HE mice compared to controls, whereas plasma ATX showed no significant difference. Enpp2 expression was upregulated 2.49-fold in salivary glands of HE mice, although salivary LPA concentrations did not differ between groups. Clinically, both serum and salivary ATX levels were significantly higher in cirrhotic patients with HE than in those without HE. Moreover, salivary ATX levels positively correlated with serum alkaline phosphatase (ALP) levels in the HE patient group. These findings demonstrate that ATX is elevated in key tissues and biofluids in both experimental and clinical HE, supporting its potential as a novel biomarker. Moreover, the data suggest that the ATX-LPA axis may contribute to HE pathophysiology, providing a foundation for future mechanistic studies and the exploration of targeted therapeutic strategies.
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6. Molecular and cellular crosstalk between atherosclerosis and cancer: Mechanistic insights and therapeutic opportunities.
PMID:日期:2026-05-31Atherosclerosis and cancer are among the leading causes of morbidity and mortality worldwide and are increasingly recognized as biologically interconnected diseases rather than independent pathological conditions. Accumulating evidence indicates that these disorders share a complex molecular landscape characterized by chronic inflammation, oxidative stress, immune dysregulation, metabolic reprogramming, endothelial dysfunction, and age-related cellular alterations. This review integrates current knowledge on the molecular and cellular mechanisms underlying the bidirectional relationship between atherosclerosis and malignancy, with particular emphasis on inflammatory signaling pathways, NLRP3 inflammasome activation, macrophage polarization, clonal hematopoiesis of indeterminate potential (CHIP), cellular senescence, and gut microbiota-mediated immune modulation. We further discuss how these shared mechanisms contribute to disease initiation, progression, and therapeutic responses, highlighting the influence of cardiovascular medications on cancer biology and the cardiovascular toxicities associated with anticancer therapies. By synthesizing emerging evidence from cardiovascular biology, oncology, and immunology, this review proposes a unified molecular framework in which atherosclerosis and cancer represent interconnected manifestations of common pathogenic processes. Recognizing this molecular crosstalk provides new opportunities for the identification of shared biomarkers, improved risk stratification, and the development of mechanism-based therapeutic strategies, thereby advancing precision medicine at the interface of cardiovascular disease and cancer.
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7. GALNS gene variants and clinical severity in pediatric mucopolysaccharidosis type IV: A retrospective cohort study from Duhok, Iraq.
PMID:日期:2026-05-31Mucopolysaccharidosis type IV (MPS IV; Morquio syndrome) is a rare lysosomal storage disorder caused by pathogenic variants in the GALNS gene, resulting in deficiency of N-acetylgalactosamine-6-sulfatase and progressive accumulation of glycosaminoglycans. The disease exhibits substantial clinical heterogeneity, and the relationship between specific GALNS variants and disease severity remains incompletely understood. This retrospective cross-sectional observational study evaluated the association between GALNS variants and clinical severity in 10 children with genetically confirmed MPS IV treated at a tertiary pediatric center in Duhok, Iraq, with data collected up to September 2025. Clinical, radiological, echocardiographic, and genetic data were retrospectively extracted from medical records. A study-derived, non-validated Clinical Severity Index (CSI; range, 0-6) was constructed from six clinically relevant skeletal, neurological, and functional manifestations, with higher scores indicating greater recorded disease burden. Three GALNS variants were identified: c.860C>T (50%), c.421T>A (30%), and c.1196delA (20%). The overall mean CSI was 2.9 ± 2.0. Patients with the frameshift variant c.1196delA had the highest mean CSI (4.0 ± 1.4), followed by c.860C>T (2.8 ± 2.6) and c.421T>A (2.3 ± 0.6); however, the difference among mutation groups was not statistically significant (Kruskal-Wallis p = 0.564). Overall, 20% of patients had mild, 50% had moderate, and 30% had severe disease according to the study-derived CSI. Multisystem involvement was common, including skeletal abnormalities in 70%, abnormal echocardiographic findings in 70%, cervical spinal cord compression in 30%, and carpal tunnel syndrome and/or communicating hydrocephalus in 40% of patients. The findings demonstrate substantial clinical variability among children with MPS IV and suggest a possible trend toward greater disease burden among patients with the frameshift variant c.1196delA, although this association was not statistically significant. Given the small sample size and the non-validated nature of the CSI, these findings should be considered exploratory and require confirmation in larger, multicenter cohorts using standardized clinical and biochemical measures.
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8. Selegiline induces neuroprotection via PGC-1α/Nrf2 gene upregulation in H2O2 -treated hippocampal-derived neural stem/progenitor cells.
PMID:日期:2026-05-31Oxidative stress mediated by reactive oxygen species (ROS) is a major contributor to the pathogenesis of neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and amyotrophic lateral sclerosis. Selegiline, a monoamine oxidase B inhibitor, has been reported to exert neuroprotective effects, although its precise cytoprotective mechanisms remain unclear. In this study, we investigated the effects of selegiline on apoptosis, necrosis, and cell survival in hydrogen peroxide (H₂O₂)-treated hippocampal-derived neural stem/progenitor cells (HD-NSPCs) in vitro. Passage 3 HD-NSPCs were treated with varying concentrations of selegiline (10⁻³ to 10⁻⁹ M) prior to exposure to 125 μM H₂O₂. Cell viability was assessed using the MTT assay, while apoptosis and necrosis were evaluated using TUNEL and acridine orange/ethidium bromide staining, respectively. Real-time RT-PCR was performed to quantify mRNA levels of PGC-1α, Nrf2, and Bcl-2. Treatment with 10⁻⁷ M selegiline significantly enhanced HD-NSC viability, reduced apoptotic and necrotic cell fractions, and upregulated PGC-1α, Nrf2, and Bcl-2 expression compared to untreated cells (P < 0.05). These findings suggest that selegiline mitigates oxidative stress-induced cytotoxicity by activating Nrf2/PGC-1α signaling and promoting anti-apoptotic gene expression, thereby preserving mitochondrial function and enhancing cell survival. Overall, selegiline may represent a promising therapeutic agent for protecting neural progenitor cells and alleviating neuronal damage in neurodegenerative disorders.
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9. NOTCH1 gene signaling pathway in the development and progression of carcinomas: an integrative review in cellular and molecular contexts.
PMID:日期:2026-04-30The NOTCH1 gene and its signaling pathway play a critical role in the oncogenesis and progression of various carcinomas through complex cellular and molecular mechanisms. This integrative literature review examines 21 selected studies across multiple carcinoma types, including head and neck, prostate, penis, breast, and hepatocellular carcinomas, to elucidate the functional impact of notch1 alterations on tumor behavior and clinical outcomes. NOTCH1 functions as a context-dependent regulator, acting either as an oncogene or tumor suppressor according to cellular environment and molecular context. Aberrations in notch1 signaling influence cell proliferation, differentiation, apoptosis, and angiogenesis, thereby contributing to cancer initiation and progression. Despite some variability in findings, the majority of studies indicate that notch1-related molecular changes have significant implications for prognosis and potential therapeutic targeting. This review highlights the importance of understanding notch1 signaling pathways in the cellular and molecular biology of carcinomas, aiming to pave the way for novel diagnostic and treatment strategies.
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10. Pomegranate seed oil combined with low-frequency electromagnetic field enhances apoptosis in HT29 colon cancer cells via modulating caspase-3, caspase-9, Bax, and Bcl-2 expression.
PMID:日期:2026-04-30Colon cancer is one of the most prevalent cancers globally, characterized by the abnormal growth of cells in the intestines. Numerous studies have explored the effects of pomegranate-derived products, such as pomegranate seed oil (PSO), as anti-proliferative, anti-invasive, and pro-apoptotic agents against various cancer cell lines. Additionally, previous research has highlighted the anti-cancer properties of low-frequency electromagnetic fields (LF-EMF). In the present study, we investigated the combined effects of these two factors on the expression of the Caspase 3, Caspase 9, BAX, and Bcl2 genes. Human colon cancer cells of the HT29 line were sourced from the Pasteur Institute of Iran cell bank and maintained in a complete culture medium. The cells were categorized into four groups: control, PSO, EMF, and PSO+EMF. To assess cell viability and the type of cell death, MTT and Annexin V-FITC assays were employed. Changes in the expression levels of Caspase 3, Caspase 9, BAX, and Bcl2 were analyzed using Real-Time PCR. The results from the MTT and Annexin V-FITC assays indicated that both PSO and EMF reduced cell viability and promoted apoptosis in colon cancer cells. The Real-Time PCR results showed an upregulation of Caspase 3, Caspase 9, and BAX genes, along with a downregulation of Bcl2 expression in the treatment groups compared to the control group. This study demonstrated that the combination of PSO and EMF enhances apoptotic gene expression, thereby diminishing the proliferation and viability of cancer cells. Based on these findings, both PSO and LF-EMF exhibit cytotoxic effects on colon cancer cells, suggesting their potential as candidates for future research in the field of colon cancer.