CELL BIOCHEMISTRY AND FUNCTION细胞生物化学与功能
CELL BIOCHEMISTRY AND FUNCTION(英文缩写 CELL BIOCHEM FUNCT),ISSN 0263-6484,eISSN 1099-0844,中文译名:细胞生物化学与功能 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：2025-09-28 至 2026-09-28，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 |
|---|---|---|
| 2021 | 3.963 | Q3 |
| 2022 | 3.600 | Q3 |
| 2023 | 2.800 | Q3 |
| 2024 | 2.700 | Q3 |
| 2025 | 3.500 | Q2 |
CELL BIOCHEMISTRY AND FUNCTION 最新收录文献
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1. Unlocking the Hepatoprotective Potential of Urolithin A in High-Fat Diet-Induced MASLD: Integrated Role of Oxidative Stress, Inflammation, FXR/PPAR-α, and Fibrotic Pathway.
PMID:日期:2026-09-01"Metabolic dysfunction-associated steatotic liver disease" (MASLD) is marked by hepatic steatosis, oxidative stress, inflammation, and fibrosis. Urolithin A (Uro A), a metabolite of ellagitannins, exhibits anti-inflammatory, antioxidant, and metabolic regulatory activities. This work examined the preventive benefits of Uro A against high-fat diet (HFD)-induced MASLD in rats and elucidated the underlying mechanisms. Four experimental groups of rats were established: control, Uro A, HFD, and HFD-Uro A. MASLD was induced by 12 weeks of HFD feeding. Uro A (2.5 mg/kg, intraperitoneally) was administered four times weekly. Metabolic indices, lipid profile, liver transaminases, oxidative stress markers, inflammatory mediators, fibrogenic markers, and hepatic farnesoid X receptor (FXR) and peroxisomal proliferator-activated receptor (PPAR)-α gene expression were evaluated. Histopathological and immunohistochemical analyses were performed. HFD significantly increased body weight, adiposity, hepatic index, transaminases, dyslipidemia, oxidative stress, inflammatory cytokines, and fibrotic markers, while downregulating FXR and PPAR-α expression. Histopathology revealed steatosis, inflammatory infiltration, and increased expression of tumor necrosis factor alpha (TNF-α), glial fibrillary acidic protein (GFAP), and Bax. Uro A markedly ameliorated metabolic, biochemical, and molecular alterations, with evident histological improvement. These findings demonstrate that Uro A exerts hepatoprotective effects against HFD-induced MASLD through integrated modulation of oxidative stress, inflammation, fibrosis, and FXR/PPAR-α pathway, bolstering its prospects as a multi-target therapeutic option for MASLD.
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2. Clerodendrum japonicum Extract Suppresses the Pathogenicity of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Inhibiting METTL3-Mediated ICAM2 mRNA Methylation.
PMID:日期:2026-09-01Clerodendrum japonicum (Thunb.) Sweet (Clerodendrum japonicum) is a traditional medicinal plant with reported anti-inflammatory use, but its anti-rheumatoid arthritis (RA) activity and molecular basis remain insufficiently characterized. Activated fibroblast-like synoviocytes (FLSs) contribute to persistent inflammation and joint destruction in rheumatoid arthritis (RA). This study investigated whether extracts of Clerodendrum japonicum attenuate pathogenic RA-FLS phenotypes and examined the possible involvement of METTL3-dependent N6-methyladenosine (m6A) regulation of ICAM2 mRNA. Tumor necrosis factor-α-stimulated human RA-FLSs (MH7A cell line) were used as an in vitro model to evaluate the anti-RA effects of Clerodendrum japonicum extracts. Cell proliferation, apoptosis, migration, invasion, and inflammatory cytokine secretion were evaluated. The underlying mechanisms were further investigated using real-time quantitative polymerase chain reaction, Western blot, and RNA immunoprecipitation. In addition, a collagen-induced arthritis (CIA) mouse model was employed to validate the anti-RA effects of the extracts in vivo. Drug-containing serum derived from Clerodendrum japonicum extracts attenuated TNF-α-induced proliferation, migration, invasion, and pro-inflammatory cytokine release in MH7A cells while increasing apoptosis. The ethyl acetate fraction (CJEA) produced the most pronounced effects among the tested fractions. CJEA-containing serum reduced global m6A abundance and METTL3 expression. METTL3 overexpression partially reversed the cellular effects associated with CJEA-containing serum. METTL3 knockdown reduced m6A enrichment and stability of ICAM2 mRNA, whereas METTL3 or ICAM2 overexpression partially restored ICAM2 expression and pathogenic RA-FLS phenotypes. Oral CJEA also reduced clinical and histological arthritis severity in CIA mice and was associated with lower synovial METTL3 and ICAM2 expression. Our findings support the involvement of METTL3-dependent m6A regulation of ICAM2 mRNA in the response of RA-FLSs to CJEA-containing serum. CJEA may attenuate pathogenic RA-FLS behavior and experimental arthritis at least partly through modulation of this pathway. Because the active constituent(s), direct molecular target, pharmacokinetics, and comprehensive safety profile remain undefined, further chemical and pharmacological validation is required.
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3. LncRNA OIP5-AS1 Promotes Glomerular Mesangial Cell Senescence by Interacting With ELAVL1 to Upregulate HMGB1.
PMID:日期:2026-09-01Glomerular mesangial cell (GMC) senescence contributes to the progression of various age-related kidney diseases. However, the molecular mechanisms driving GMC aging remain poorly understood. OIP5-AS1, a long non-coding RNA (lncRNA), has been implicated in cellular senescence in other systems, but its role in renal aging remains unclear. This work aimed to elucidate the functional role and underlying mechanism of OIP5-AS1 in GMC senescence. A D-galactose (D-gal)-induced senescence model was established in both mouse kidneys and SV40-MES13 mesangial cells. RT-qPCR was performed to quantify the levels of OIP5-AS1, ELAVL1, and HMGB1, while CCK-8 assays assessed cellular metabolic activity. Cellular senescence was evaluated using SA-β-gal staining, and the expression of senescence-associated proteins (p16, p21, p53) was quantified by Western blot analysis. Levels of SASP-related cytokines, including IL-6, IL-1β, TNF-α, and IL-18, were measured via ELISA. To explore the underlying mechanism, RNA pull-down and RIP assays were performed to investigate the interactions among OIP5-AS1, ELAVL1, and HMGB1, while actinomycin D assays were used to evaluate HMGB1 mRNA stability. OIP5-AS1 expression was markedly elevated in renal tissues and GMCs following D-gal-induced senescence. Knockdown of OIP5-AS1 alleviated cellular senescence. Mechanistically, OIP5-AS1 directly interacted with ELAVL1, thereby stabilizing HMGB1 mRNA and promoting HMGB1 expression. Rescue experiments further confirmed that ELAVL1 and HMGB1 mediated OIP5-AS1-induced GMC senescence. LncRNA OIP5-AS1 promotes GMC senescence by interacting with ELAVL1 to upregulate HMGB1.
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4. Mechanistic Pathways of Wound Healing: From Hemostasis to Scar-Free Regeneration.
PMID:日期:2026-09-01Wound healing is the critical process regulated through a harmonious coordination of cellular, molecular, pathological, and systemic communications. Normally, healing occurs in four overlapping phases, which are modified and controlled by various growth factor interactions and signaling pathways. Disruption of the tightly coordinated wound-healing cascade, together with aberrant protein signaling, mitochondrial dysfunction, antimicrobial resistance, sustained fibroblast activation, and maladaptive epigenetic reprogramming, drives pathological tissue repair culminating in chronic non-healing wounds, including diabetic, ischemic, and venous ulcers, as well as fibrotic outcomes such as hypertrophic and keloid scarring. The persistent fibroblast activation, reduced apoptosis, prolonged TGF-β activity, and severe fibrosis induced by mechanical methods trigger excessive healing, while existing therapies fail to manage these functions. Therefore, in order to develop advancements toward precise and personalized medicine, it is important to understand the various mechanisms involved in wound healing. The current review provides a comprehensive understanding of various fundamental mechanisms involved in wound healing, such as cellular, molecular, signaling pathways, genetic, epigenetic, pathological, immunological, and systemic mechanisms. Knowledge of these mechanisms and how they work under physiological as well as pathological conditions connects to clinical inefficiency, which helps to provide accurate medicine. A deeper mechanistic knowledge paves the way for developing innovative biomaterials; nanotechnology-based therapeutic strategies, specific drug delivery, molecular biomarkers, and scar-free healing of wounds, which enrich the future with advanced therapeutics and personalized medicine for wounds.
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5. USP18 Serves as a Key Mediator of cGAS-STING for Cardiac Aging in Diabetes.
PMID:日期:2026-09-01Diabetes accelerates cardiac aging, but the molecular mechanisms that link metabolic stress to myocardial senescence remain insufficiently defined. This study investigated factors driving diabetes-associated cardiac aging with a focus on the role of USP18. Type 2 diabetes mellitus (T2DM) was induced in mice using a high-fat diet combined with streptozotocin. Cardiac structure, function, and molecular alterations were evaluated by echocardiography, histology, RNA sequencing, western blotting, qPCR, and immunofluorescence. H9C2 cardiomyocytes cultured under high-glucose conditions were used for in vitro validation. Diabetic mice exhibited diastolic dysfunction, myocardial hypertrophy, and fibrosis, accompanied by increased p53 and p21 expression. RNA-seq and protein analyses consistently identified USP18 as significantly upregulated in diabetic hearts. Elevated USP18 was associated with activation of the cGAS-STING pathway, increased TBK1 phosphorylation, and enhanced IL-6 and IL-1β production. High-glucose-treated cardiomyocytes similarly showed USP18 induction, stabilization of cGAS-STING signaling, and enhanced senescence-related responses. USP18 contributes to cardiac aging in diabetes by promoting cGAS-STING activation and inflammatory senescence. Targeting USP18 may represent a potential strategy to alleviate myocardial aging under diabetic conditions.
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6. Cytotoxic Effects of Medicinal Plant Extracts on HeLa Cells via Redox Imbalance, L-Arginine Metabolic Reprogramming, and Glycolytic Suppression.
PMID:日期:2026-09-01Cancer cells undergo metabolic reprogramming to sustain proliferation, resist apoptosis, and adapt to oxidative stress. In the present study, we comparatively evaluated the anticancer effects of four medicinal plant extracts (Inula helenium, Hypericum alpestre, Rumex obtusifolius, and Alchemilla smirnovii) on HeLa cervical cancer cells, with particular emphasis on oxidative stress, l-arginine metabolism, and cellular energy pathways. Cell viability was assessed using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, while biochemical colorimetric methods were used to determine nitric oxide production, arginase and nitric oxide synthase activities, malondialdehyde levels, superoxide dismutase and catalase activities, proline content, and key glycolytic metabolites. Nuclear morphology changes consistent with apoptotic features were examined by Hoechst 33258 staining. All tested extracts exhibited cytotoxic effects in HeLa cells in a time- and concentration-dependent manner, which were further enhanced when combined with the metabolic inhibitors l-NAME (Nω-nitro-l-arginine methyl ester) or nor-NOHA (Nω-hydroxy-nor-l-arginine). Inula helenium showed the strongest potentiation in combination treatments. Several extracts significantly decreased arginase activity while increasing nitric oxide synthase activity and nitrite levels, indicating modulation of l-arginine metabolism. Treatments also increased malondialdehyde levels and stimulated antioxidant enzyme activities, consistent with redox imbalance and oxidative stress-mediated cytotoxicity. In addition, Inula helenium and Alchemilla smirnovii reduced intracellular glucose, pyruvate, and lactate concentrations, suggesting partial modulation of glycolytic metabolism. Fluorescence microscopy revealed chromatin condensation, nuclear fragmentation, and apoptotic body formation, particularly after treatment with Hypericum alpestre and Rumex obtusifolius. These findings demonstrate that selected medicinal plant extracts exert cytotoxic effects by simultaneously modulating oxidative stress, amino acid metabolism, and energy pathways in cervical cancer cells. The investigated plants may represent promising sources of bioactive compounds for the development of complementary metabolic anticancer strategies.
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7. Melatonin Regulates Growth-Arrest and DNA-Damage Genes GADD153, GADD45g and GADD34 in Experimental Varicocele.
PMID:日期:2026-09-01This study aimed to reveal the relationship between experimental varicocele and melatonin levels. Forty adult Wistar albino rats were used in this study. Control (C), Melatonin (M), Varicocele (V), Varicocele+Melatonin (V + M) were planned. Varicocele was created on the first day of the experiment by opening the abdominal area, narrowing the left renal vein with a 0.85 mm metal wire and using a 4-0 silk suture, after removing the metal wire, the animal was closed (with a 3-0 silk suture) and kept for 60 days. Melatonin was administered at 10 mg/kg ip (intraperitoneal) on the 61st day, every 24 h for 7 days. Histological analysis and GADD34, GADD45g, GADD153 immunohistochemical staining were performed. Additionally, StAR and GDNF gene expressions were examined. ABP, FSH, LH, Testosterone, Melatonin hormones, TAS and TOS levels were evaluated from blood serum taken from experimental animals. According to our results, group V showed a decrease in testicular weights, seminiferous tubule diameter, and JTBS score, while GADD34, GADD45g and GADD153 proteins increased. In group V, testosterone and TAS levels decreased and TOS levels increased. In group V, testosterone, FSH, ABP, melatonin levels decreased and LH level increased. StAR and GDNF gene expression also decreased in group V. In the V + M group where melatonin was applied, an improvement was observed in biochemical parameters as well as histological, immunohistochemical and gene expression analyses. During varicocele, endogenous melatonin level decreases and activates various mechanisms and hormones in the tissue, including GADDs, causing loss of structure and function, while melatonin acts as a good therapeutic on varicocele.
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8. Microproteins as a Hidden Player in Breast Cancer: From Molecular Insights to Therapeutic Potential.
PMID:日期:2026-09-01Breast cancer continues to pose a public health problem and is the second leading cause of cancer-related mortality among women globally. Despite advances in our understanding of cancer biology and the development of treatment strategies, the therapeutic response is not often satisfactory as treatment efficacy is limited by severe side effects and drug resistance. Therefore, there is an urgent need for innovative approaches to improve diagnosis, prognosis, and treatment of breast cancer. Recent advances in bioinformatics and proteomics have enabled the discovery of a novel class of small proteins encoded from the small open reading frames, which were previously thought to be non-coding. Emerging evidence has indicated that these microproteins play a pivotal role in modulating breast cancer progression. This article reviews the current understanding of microproteins, highlights the microproteins identified to date as key regulators in breast cancer, and explores their potential clinical applications in improving breast cancer management.
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9. Analysis of the Role of N-Linked Glycans on Human CD1d Molecules.
PMID:日期:2026-09-01CD1d is a cell-surface expressed glycoprotein that presents a variety of lipid and glycolipid antigens to invariant natural killer T-cells (iNKT). We have examined the role of the N-linked glycans on the human CD1d (hCD1d) in modulating the responses of iNKT cells using a combination of cell-free, cell-based assays and in silico analyses. Deficiency of one or more glycans on hCD1d diminished the activation of iNKT cells. Soluble glycan mutants did not have significant differences in terms of binding to the nickel-coated 96-well plates. Our cell-free assay, together with docking and MM-GBSA analyses, confirms that Glycan 1 and Glycan 2 are critical determinants of optimal iNKT cell activation. Taken together, our data emphasized an essential role of the hCD1d N-linked glycans in modulating iNKT cell response.
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10. Melatonin Protects BEAS-2B Cells Against Hypoxia/Reoxygenation-Induced Injury By Reducing MLKL Levels, Suppressing Oxidative Stress and Preserving Mitochondrial Function.
PMID:日期:2026-09-01Necroptosis has been demonstrated to play a role in the process of lung ischemia-reperfusion injury (LIRI) in a variety of clinical conditions, including cardiopulmonary bypass and pulmonary embolism. Melatonin has been reported to exert a protective role by reducing oxidative stress and acute inflammatory reactions in LIRI. However, the effect of melatonin on necroptosis in LIRI remains unclear. The aim of this study was to investigate whether the protective effects of melatonin against H/R-induced injury are associated with modulation of necroptosis and related changes in mitochondrial function and oxidative stress. The cells were exposed to H/R (16/4 h) or normoxia, in the absence or presence of 2.5 µM melatonin. Cell viability was determined by the MTT method, while morphological changes in BEAS-2B cells resulting from H/R exposure were evaluated by fluorescence microscopy using acridine orange/ethidium bromide (AO/EtBr) staining. Mechanistic analyses, including flow cytometry-based cell cycle assessment, apoptosis detection (Annexin V-FITC), mitochondrial membrane potential evaluation (JC-1), and reactive oxygen species (ROS) measurements, were performed on BEAS-2B cells. The level of the mixed lineage kinase domain-like pseudokinase (MLKL), a key component of the necroptosis complex, was also quantified using an enzyme-linked immunosorbent assay. In addition, the ATP, pH, and lactate levels were determined. The findings indicated that melatonin treatment reduced the H/R-induced increase in the percentage of necrotic cells and increased the percentage of viable cells (p < 0.05). In addition, melatonin treatment reduced the increase in MLKL, ROS, and lactate levels, preserved mitochondrial membrane integrity, and increased intracellular ATP levels in BEAS-2B cells exposed to H/R (p < 0.05). In conclusion, this study suggests that melatonin protects BEAS-2B cells against H/R-induced injury, and that this protective effect may be associated with reduced oxidative stress, preservation of mitochondrial function, and suppression of necroptosis-related signaling.