细胞生理学和生物化学是一个致力于推进基础细胞研究前沿的多学科科学论坛。它面向来自生理和生化学科以及遗传学、分子生物学、病理生理学、病理生物化学和细胞毒理学和药理学等相关领域的科学家。发表了关于细胞内传递、细胞代谢、细胞生长、分化和死亡、离子通道和载体以及细胞体积的维持、调节和干扰的机制的原创论文和综述。细胞生理学和生物化学每月都会在同行评审下出现，在国际社会共同努力解开细胞功能机制方面发挥了积极作用。

Cellular Physiology and Biochemistry is a multidisciplinary scientific forum dedicated to advancing the frontiers of basic cellular research. It targets scientists from various fields, including physiology, biochemistry, genetics, molecular biology, pathophysiology, pathobiochemistry, cytotoxicology, and pharmacology. The journal publishes original papers and reviews on mechanisms of intracellular signaling, cellular metabolism, growth, differentiation, and death, as well as the maintenance, regulation, and disruption of cell volume, ion channels, and carriers. It is published monthly and undergoes peer review, playing an active role in the international community's efforts to unravel the mechanisms of cellular function.

《Cellular Physiology and Biochemistry》是一个多学科科学论坛，致力于推动基础细胞研究的前沿。该期刊面向来自生理学、生物化学、遗传学、分子生物学、病理生理学、病理生物化学、细胞毒理学和药理学等相关领域的科学家。期刊发表原创论文和综述，内容涵盖细胞内信号传递、细胞代谢、细胞生长、分化与死亡、离子通道和载体的机制，以及细胞体积的维持、调节和干扰等方面。每月定期出版，并经过同行评审，为国际科学界共同揭示细胞功能机制做出了积极贡献。

Cellular Physiology and Biochemistry

Background/Aims: Urothelial carcinoma-associated 1 (UCA1) is a recently identified long non coding RNA (lncRNA). However, few studies have explored its role in cardiomyocytes after focal cardiac ischemia reperfusion injury (CIR). Methods: Rat CIR models were established using ligation of the Lower Anterior Descending artery (LAD). Cell apoptosis and reactive oxygen species (ROS) production in cardiac tissues were explored using immunohistochemistry and DHE staining. lncRNA expression patterns were detected using microarray and validated by qPCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. Results: CIR significantly induced cell apoptosis and ROS production in the rat model. The results of microarray demonstrated the reduced expression of UCA1, which was validated by qPCR. Follow-up experiments showed that UCA1 was involved in H2O2-induced cell apoptosis. We further showed that UCA1 negatively correlated with the expression of p27. Moreover, overexpression of p27 could induce primary cardiomyocyte apoptosis. Conclusions: Reduction of UCA1 levels plays a pro-apoptotic role in primary cardiomyocytes partially through stimulation of p27 protein expression. These results are in agreement with the observed levels of UCA1, p27 and apoptosis after cardiac I/R injury, suggesting that UCA1 might have an important role during I/R injury.

Youbin Liu

Daliang Zhou

Guangnan Li

Xing Ming

Ying feng Tu

Jinwei Tian

Huimin Lu

Bo Yu

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Neutrophils were traditionally considered as short-lived cells with abundant secretory and protein synthetic activity. Recent studies, however, indicate neutrophils are in reality a heterogeneous population of cells. Neutrophils differentiate from pluripotent stem cells in the bone marrow, and can further mature in the blood stream and can have different phenotypes in health and disease conditions. Neutrophils undergo primary functions such as phagocytosis, production of reactive oxygen species (ROS), release of lipid mediators and inflammatory proteins (mainly cytokines), and apoptosis. Neutrophils stimulate other neutrophils and trigger a cascade of immune and inflammatory responses. The underpinning intracellular metabolisms that support these neutrophil functions are herein reported. It has been known for many decades that neutrophils utilize glucose as a primary fuel and produce lactate as an end product of glycolysis. Neutrophils metabolize glucose through glycolysis and the pentose- phosphate pathway (PPP). Mitochondrial glucose oxidation is very low. The PPP provides the reduced nicotinamide adenine dinucleotide phosphate (NADPH) for the NADPH-oxidase (NOX) complex activity to produce superoxide from oxygen. These cells also utilize glutamine and fatty acids to produce the required adenosine triphosphate (ATP) and precursors for the synthesis of molecules that trigger functional outcomes. Neutrophils obtained from rat intraperitoneal cavity and incubate for 1 hour at 37°C metabolize glutamine at higher rate than that of glucose. Glutamine delays neutrophil apoptosis and maintains optimal NOX activity for superoxide production. Under limited glucose provision, neutrophils move to fatty acid oxidation (FAO) to obtain the required energy for the cell function. FAO is mainly associated with neutrophil differentiation and maturation. Hypoxia, hormonal dysfunction, and physical exercise markedly change neutrophil metabolism. It is now become clear that neutrophil metabolism underlies the heterogeneity of neutrophil phenotypes and should be intense focus of investigation.

Rui Curi

Adriana Cristina Levada-Pires

Eliane Borges da Silva

Sarah de Oliveira Poma

Raquel Freitas Zambonatto

Paola Domenech

Mariana Mendes de Almeida

Raquel Bragante Gritte

Talita Souza-Siqueira

Renata GorjÃ£o

Philip Newsholme

Tania Cristina Pithon-Curi

Cell Physiol Biochem

The Critical Role of Cell Metabolism for Essential Neutrophil Functions

Propolis is one of the most promising natural products, exhibiting not only therapeutic but also prophylactic actions. Propolis has several biological and pharmacological properties, including hepatoprotective activities. The present study aimed to investigate the underlying molecular mechanisms of propolis against CCl4-mediated liver fibrosis.Three groups of male BALB/c mice (n=15/ group) were used: group 1 comprised control mice; groups 2 and 3 were injected with CCl4 for the induction of liver fibrosis. Group 3 was then orally supplemented with propolis (100 mg/kg body weight) for four weeks. Different techniques were used to monitor the antifibrotic effects of propolis, including histopathological investigations using H&E, Masson's trichrome and Sirius red staining; Western blotting; flow cytometry; and ELISA.We found that the induction of liver fibrosis by CCl4 was associated with a significant increase in hepatic collagen and α-smooth muscle actin (α-SMA) expression. Moreover, CCl4-treated mice also exhibited histopathological alterations in the liver architecture. Additionally, the liver of CCl4-treated mice exhibited a marked increase in proinflammatory signals, such as increased expression of HSP70 and increased levels of proinflammatory cytokines and ROS. Mechanistically, the liver of CCl4-treated mice exhibited a significant increase in the phosphorylation of AKT and mTOR; upregulation of the expression of BAX and cytochrome C; downregulation of the expression of Bcl2; a significant elevation in the levels of TGF-β followed by increased phosphorylation of SMAD2; and a marked increase in the expression of P53 and iNOS. Interestingly, oral supplementation of CCl4-treated mice with propolis significantly abolished hepatic collagen deposition, abrogated inflammatory signals and oxidative stress, restored CCl4-mediated alterations in the signaling cascades, and hence repaired the hepatic architecture nearly to the normal architecture observed in the control mice.Our findings revealed the therapeutic potential and the underlying mechanisms of propolis against liver fibrosis.

Gamal Badr

Eman Abdo Sayed

Hanan Waly

Khadiga Abdel-Hameed Hassan

Mohamed H Mahmoud

Zeliha Selamoglu

The Therapeutic Mechanisms of Propolis Against CCl4-Mediated Liver Injury by Mediating Apoptosis of Activated Hepatic Stellate Cells and Improving the Hepatic Architecture through PI3K/AKT/mTOR, TGF-β/Smad2, Bcl2/BAX/P53 and iNOS Signaling Pathways

The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway.Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy.In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression.The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

Xuan Ye

Qiong Du

Bin Zhu

Qing Zhai

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

长链非编码RNA CRNDE通过竞争性结合miR-217与TCF7L2并增强Wnt/β-Catenin信号通路促进结直肠癌进展

Yes-associated protein (YAP) is one of the Hippo pathway's two effectors, a pathway associated with organ size control. Research on YAP has focused on its oncogenic potential. However, in cancer cells, aside from inducing growth, YAP was also found to regulate glucose metabolism. Therefore, we aimed to explore YAP's control of glucose metabolism and whether these findings are translatable to physiological conditions. We conducted a systematic review of the MEDLINE database through PubMed in April 2020 and repeated the search in September 2020. We found that YAP induced the transcriptional activity of most genes associated with glucose metabolism from enzymes to transport proteins. In glycolysis and gluconeogenesis, YAP upregulated all enzymes except for enolase and pyruvate kinase. Multiple research has also shown YAP's ability to regulate the expression of glucose transporter of the GLUT family. Additionally, glucose concentration, hypoxia, and hormones such as insulin and glucagon regulate YAP activity and depend on YAP to exert their biological activity. In this review, we have shown that YAP is a central regulator of glucose metabolism, controlling both enzymes and proteins involved in glucose transport. YAP is also situated strategically in several pathways controlling glucose and was found to mediate their effects. If these results were consistent in physiological conditions and across glucose-associated metabolic disturbances, then YAP may become a prospective therapeutic target.

Ardo Sanjaya

Hanna Goenawan

Iwan Setiawan

Julia Windi Gunadi

Yenni Limyati

Ronny Lesmana

Elaborating the Physiological Role of YAP as a Glucose Metabolism Regulator: A Systematic Review

阐述YAP作为葡萄糖代谢调节因子的生理作用：一项系统综述

Tendons play a crucial role in the musculoskeletal system, connecting muscles to bones and enabling efficient force transfer. However, they are prone to acute and chronic injuries, which, if not properly repaired, can significantly impair function. Tendinopathy, a prevalent condition affecting approximately 20% of musculoskeletal complaints, arises from an imbalance between micro-injury accumulation and repair processes. The extracellular matrix (ECM) of tendons is a hierarchical structure comprising collagen fibrils, proteoglycans, and glycoproteins that regulate organization, hydration, and mechanical properties. Mechanotransduction pathways, mediated by integrins and focal adhesion complexes, activate signaling cascades such as MAPK/ERK and PI3K/Akt, driving tenocyte gene expression and ECM remodeling. Adaptations to load involve region-specific remodeling, with tensile regions favoring aligned Type I collagen and compressive regions promoting proteoglycans like aggrecan. Stress shielding or reduced loading disrupts these pathways, leading to matrix disorganization and inflammation, predisposing tendons to degenerative changes. Insights into these molecular mechanisms inform rehabilitation strategies to enhance tendon repair and mitigate tendinopathy progression in both athletic and general populations.

Mikołaj Stańczak

Bartłomiej Kacprzak

Piotr Gawda

Tendon Cell Biology: Effect of Mechanical Loading

肌腱细胞生物学：机械负荷的影响

The nano-method has been used as a technique for creating novel, non-traditional antimicrobial agents. This effective method for treating infectious diseases has many advantages over conventional antibiotics, including increased efficacy against species that have developed drug resistance, and the ability to circumvent the development of resistance that disrupts a number of biological pathways. As a result, the objective of this study was to synthesize and characterize silver nanoparticles using phenolic compounds obtained from

Hawazen Salih

Rami Altameemi

Ahmed Al-Azawi

Antibacterial Activity of Silver Nanoparticles Prepared from Camellia Sinensis Extracts in Multi-Drug Resistant Staphylococcus Aureus

茶树提取物制备的银纳米粒子对耐多药金黄色葡萄球菌的抗菌活性

Background/Aims: Lead exposure is known to induce oxidative stress and neurotoxicity. Nitric oxide (NO) plays an important role in modulating oxidative stress, with L-arginine as a precursor of NO and Nω-nitro-L-arginine (L-NNA) as an inhibitor of NO synthase, an enzyme that catalyses the production of nitric oxide (NO) from L-arginine. Methods: This study investigated the differential effects of L-arginine and L-NNA on markers of oxidative stress and biochemical changes in brain tissue from rats with different levels of resistance to hypoxia exposed to lead nitrate. Rats with either low or high resistance to hypoxia were exposed to lead nitrate (oral 3.6 mg lead nitrate/kg b.w. per day for 30 days) and treated with L-arginine (600 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate) or L-NNA (35 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate). Brain tissue samples were analysed for lipid peroxidation, oxidative modification of proteins, and activity of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, and peroxidase, and total antioxidant status (TAS). We also examined the biomarkers of biochemical pathways involving the activity of alanine and aspartate aminotransferases, succinate dehydrogenase (SDH), and α-ketoglutarate dehydrogenase (KGDH). In addition, the trend observed was supported by assessments of the acetylcholine levels and acetylcholinesterase activity (ACh-AChE system) in brain tissue. Results: In rats with low resistance to hypoxia, the L-arginine treatment significantly reduced lipid peroxidation and oxidative protein modification but increased antioxidant enzyme activity, suggesting a protective effect against lead-induced oxidative stress. Conversely, in rats with high resistance to hypoxia, L-NNA had a protective effect, reducing lead-induced oxidative damage and decreasing lipid peroxidation, whereas L-arginine exacerbated oxidative stress and impaired antioxidant defences. These findings were supported by corresponding changes in the acetylcholine-acetylcholinesterase system, reflecting the observed patterns of lead-induced oxidative stress and neurotoxicity. The study shows that L-arginine exerts a protective effect by reducing lead-induced oxidative damage via an improvement in TAS. Our study shows that lead nitrate exposure significantly increases ala-nine and aspartate aminotransferase activity in brain tissue, with L-arginine exacerbating and L-NNA reversing this effect. The lead nitrate exposure also affected the activities of SDH and KGDH, which are important for cellular energy production and hypoxia resistance, with L-arginine altering SDH activity depending on the level of resistance and L-NNA enhancing both SDH and KGDH activities. These trends were further validated by alterations in the ACh-AChE system, highlighting the differential role of NO-dependent mechanisms in modulating lead-induced neurotoxicity based on hypoxia resistance. Conclusion: These findings suggest potential targeted therapeutic strategies based on the oxidative stress profile and highlight the potential of nitric oxide system modulators in counteracting lead-induced biochemical alterations and the dynamics of the ACh-AChE system depending on the individual physiological reactivity of organisms.

Natalia Kurhaluk

Piotr Kamiński

Oleksandr Lukash

Halina Tkaczenko

Nitric Oxide-Dependent Regulation of Oxygen-Related Processes in a Rat Model of Lead Neurotoxicity: Influence of the Hypoxia Resistance Factor

一氧化氮依赖性调节氧相关过程在大鼠铅神经毒性模型中的作用：缺氧抵抗因子的影响

Breast cancer is the most frequent cancer among women. Despite extensive research in recent years the molecular basis of breast cancer development, growth and metastasis remains unclear. Numerous studies highlight the involvement of BMI-1 in tumorigenesis. BMI-1 protein is a key component of Polycomb Repressive Complex 1, which by ubiquitinylation of histone H2A, regulates expression of genes involved in various cellular processes including cell cycle, proliferation and programmed cell death. Overexpression of BMI-1 has been often associated with breast cancer development and progression. This review summarizes the current state of knowledge of BMI-1's role in breast cancer biology and its potential significance as prognostic marker and potential target of new anticancer therapy.

Aleksandra Szustka

Anna Krześlak

BMI-1 in Breast Cancer – Biological Role and Clinical Implications

BMI-1在乳腺癌中的生物学作用及临床意义

Background/Aims: Atherosclerotic cardiovascular disease (ASCVD) or atherosclerosis is a chronic condition that is incurable and a leading contributor to morbidity and mortality. However, it is easy to prevent ASCVD by managing or preventing risk factors like hyperlipidemia, obesity/overweight, hypertension, and diabetes. This systematic review summarizes and presents current evidence on whether physical exercise could help in reducing ASCVD risk factors. Materials: A comprehensive search was performed on PubMed, CINAHAL, ProQuest and Google Scholar. The sources were assessed based on their peer-review status, description of methods, unavailability of full texts, publication date (less than seven years), and publication in the English Language. The final search results constituted 19 peer-reviewed articles. Results: Physical exercise is effective in improving the lipid profile, reducing waist circumference, reducing blood pressure, and lowering blood glucose levels. All types of physical exercise with intensity varying from low to high yield positive outcomes, although there is no consensus on whether the physical exercise program should be implemented for three months or less or on a long-term basis. Conclusion: Physical exercise prevents and improves the management of hyperlipidemia, obesity/overweight, hypertension, and diabetes, which makes it a good intervention for reducing the risk of ASCVD. However, further studies should be performed to determine the duration within which the intervention should be sustained for optimal results.

Nada Alhazmi

The Effectiveness of Physical Exercise in Reducing Common Risk Factors of Atherosclerosis: A Systematic Review

体力活动在降低动脉粥样硬化常见风险因素中的有效性：一项系统综述

Abbreviation	Cell Physiol Biochem
Journal Impact	2.44
Quartiles(Global)	PHYSIOLOGY(Q2)

ISSN	1015-8987, 1421-9778
h-index	112

Publication Information	Publisher: Cell Physiol Biochem Press GmbH & Co KG，Publishing cycle: Bimonthly，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 1991，Proportion of original research papers: 0.00%，Self Citation Rate:4.00%， Gold OA Rate: 98.73%
Journal Fees	$Details
Average review cycle	网友分享经验：平均1月
Average recruitment ratio	网友分享经验：约95%

Cellular Physiology and Biochemistry

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