Cell Biochemistry and Biophysics最新文献

{"title":"In Vitro COX Inhibitory Activity, LC-MS Analysis and Molecular Docking Study of Silene vulgaris and Stellaria media.","authors":"Pooja Chak, Akansha Bisht, Deepti Choudhary, Smita Jain, Priyanka Joshi, Sonika Jain, Pankaj Jain, Jaya Dwivedi, Swapnil Sharma","doi":"10.1007/s12013-024-01533-0","DOIUrl":"10.1007/s12013-024-01533-0","url":null,"abstract":"<p><p>Silene vulgaris (Moench) Garcke and Stellaria media (L.) Vill is a perennial wild weed species belonging to the Caryophyllaceae family and is widely available and abundant in the environment. The present study has aimed to evaluate the anti-inflammatory potential of two underutilized wild edible plants, Silene vulgaris (Moench) Garcke and Stellaria media (L.) Vill. fractions employing in-vitro COX inhibitory assay. Invitro COX-2 inhibitory potential of MESV and MESM fractions was carried out using BioVision^R \"COX Activity Assay Kit (Fluorometric)\". LC-MS analysis of selected fractions was conducted to identify bioactive compounds that were further validated for their affinity determination toward target enzymes employing molecular docking studies using the LibDock program. In-vitro COX inhibitory assay revealed that hexane fraction of S. vulgaris (HFSV) and hexane fraction of S. media (HFSM) caused impressive inhibition of COX-2 enzyme with IC₅₀ values 1.38 µg/mL and 1.51 µg/mL respectively. Further, LC-MS analysis revealed the presence of 46 compounds in HFSV and 44 compounds in HFSM respectively. Amongst identified bioactive compounds in HFSV and HFSM, sinapinic acid and syringic acid showed good docking scores with COX-2 i.e., 89.256, and 82.168 respectively. Also, the availability of chrysin in HFSM and rhamnetin in HFSV exhibited good docking scores i.e., 115.092, and 112.341 with a selective affinity towards COX-2. The findings of in-vitro COX Inhibitory Activity and molecular docking studies highlighted the impressive anti-inflammatory properties of S. vulgaris and S. media, and require further investigations to establish them as therapeutic candidates in the management of inflammation and related issues.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"1009-1020"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142306879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Expression of Nemo-Like Kinase (NLK) in the Brain in a Rat Experimental Subarachnoid Hemorrhage Model.","authors":"Gang Chen, Dongxia Feng, Li Zhang, Baoqi Dang, Huixiang Liu, Zhong Wang","doi":"10.1007/s12013-024-01523-2","DOIUrl":"10.1007/s12013-024-01523-2","url":null,"abstract":"","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"1327-1328"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Passion Fruit Seed Extract Attenuates Hepatic Steatosis in Oleic Acid-Treated HepG2 Cells through Modulation of ERK1/2 and Akt Signaling Pathways.","authors":"Furoida Moolsup, Wiwit Suttithumsatid, Wanwipha Woonnoi, Pennapa Chonpathompikunlert, Supita Tanasawet, Wanida Sukketsiri","doi":"10.1007/s12013-025-01706-5","DOIUrl":"https://doi.org/10.1007/s12013-025-01706-5","url":null,"abstract":"<p><p>Hepatic steatosis, commonly referred to as fatty liver disease, is defined by the abnormal buildup of fat within liver cells. Currently, primary treatments mainly focus on lifestyle changes, underscoring a lack of direct pharmacological options. Passion fruit seed extract (PFSE) has been reported to decrease hepatosteatosis; however, the mechanism underlying this effect has not been clarified. Therefore, the objective of this research was to investigate the effects and mechanisms of action of PFSE against oleic acid (OA)-induced hepatosteatosis in HepG2 cells. OA-induced HepG2 cells were analyzed by using various cell-based experiments, including assessments of cytotoxicity, reactive oxygen species (ROS) production, apoptosis, and protein and gene expression. LC-MS-MS analysis showed that PFSE contains a variety of phytochemical compounds such as alkaloids, flavonoids, stilbenoids, coumarins, terpenoids, lipids, and fatty acid derivatives, which have the potential to exhibit various pharmacological activities. In this study, PFSE demonstrated antioxidant, anti-inflammatory, and lipid metabolism-regulating activities. It also influenced key genes related to lipid metabolism, including SREBP-1c, ACC, FASN, PPARα, CPT-1A, LPL, SCD1, and LDLR. The positive effects of PFSE on OA-induced hepatic steatosis in HepG2 cells were modulated through the Akt and ERK signaling pathways, suggesting that PFSE may offer a comprehensive approach to managing hepatic steatosis.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory Roles and Therapeutic Potential of miR-122-5p in Hypoxic-Ischemic Brain Injury: Comprehensive Review.","authors":"Abdulaziz S Bamahel, Xun Sun, Wei Wu, Chenxi Mu, Jia Liu, Sheng Bi, Hui Xu","doi":"10.1007/s12013-025-01686-6","DOIUrl":"https://doi.org/10.1007/s12013-025-01686-6","url":null,"abstract":"<p><p>In the regulation of gene expression, epigenetic factors, including non-coding RNAs (ncRNAs) play a role in genetics. Among the ncRNA family, microRNAs (miRNAs) have gained significant attention for their involvement in post-transcriptional gene regulation, with profound implications for both normal and pathological processes including neurological diseases such as hypoxic-ischemic brain injury. A specific miRNA, called miR-122-5p, has gained attention in hypoxic-ischemic conditions, where it modulates critical pathways such as inflammation, oxidative stress, and neuronal survival. The purpose of this review is to highlight recent advances in the biogenesis, expression, and regulation of miR-122-5p, focusing on its role in hypoxic-ischemic conditions and its potential as a therapeutic target. We first studied the therapeutic strategies and potential clinical applications of miR-122-5p, our research showing it interacts with key transcription factors, such as HIF-1α and NF-κB, influencing cellular responses to low oxygen levels. Our findings revealed that miR-122-5p plays a vital role in hypoxic-ischemic brain injury, with its abnormal levels strongly associated with increased brain damage and neuroinflammation, suggesting its potential as a promising therapeutic target. Furthermore, miR-122-5p influences various biological processes in the brain, such as metabolism and blood vessel formation. The use of miR-122-5p inhibitor has been shown to increase autophagy, reduce apoptosis, and decrease oxidative stress and inflammation, thereby protecting neurons and improving outcomes in hypoxic encephalopathy by targeting multiple genes related to these processes. Conversely, miR-122-5p mimics exacerbate oxidative stress and reduce autophagy. These findings highlight the therapeutic potential of miR-122-5p inhibition in reducing brain injury and promoting recovery in hypoxic-ischemic encephalopathy through enhanced neuroprotective mechanisms and the suppression of harmful cellular processes. However, further experimental studies are needed to fully understand the therapeutic potential of targeting miR-122-5p and its related genes in hypoxic-ischemic encephalopathy.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Epicatechin on the Expression of MyomiRs-31, -133, -136, -206, -296, and -486 in the Skeletal Muscle of the Offspring of Obese Mothers.","authors":"Paola B Zárate-Segura, Ana Luisa Alvarez-Chávez, Sergio De Los Santos, Fernando G Bastida-Gonzalez, José Manuel Hernández-Hernández, Elena Zambrano, Ramón Mauricio Coral-Vázquez, Patricia Canto","doi":"10.1007/s12013-025-01700-x","DOIUrl":"https://doi.org/10.1007/s12013-025-01700-x","url":null,"abstract":"<p><p>Specific myogenic microRNAs termed \"myomiRNAs\" are involved in skeletal muscle development and regeneration, and an obesogenic environment in utero may affect these processes. The present study aimed to determine whether this environment induced variations in the expression levels of myomiRs-31, -133, -136, -206, and -296 and whether the administration of (-)-epicatechin (Epi), an exercise mimetic, could modify these variations. Rat Wistar male offspring from control mothers (C) or obese mothers (MO) were treated (C+Epi and MO+Epi) or not treated with Epi (C and MO). MyomiRNA expression in the gastrocnemius and soleus muscles was analyzed via RT‒qPCR, and bioinformatic analysis was used to predict the participation of these miRNAs in different skeletal muscle signal transduction pathways. The expression of myomiRNA-31-5p in the gastrocnemius and soleus was significantly lower in the Epi-treated groups (C+Epi and MO+Epi vs. C and MO). The expression of myomiRNA-206 increased in the gastrocnemius muscles of the MO and MO+Epi groups but decreased in the soleus muscles of the MO and MO+Epi groups. The expression of myomiRNA-296 was increased in the MO group in the gastrocnemius and soleus but was reduced in the Epi stimulus group. The expression of myomiRNA-486 increased in the gastrocnemius of the C+Epi group and decreased in the soleus of the MO+Epi group (p = 0.028 vs. MO). In conclusion, we show that an intrauterine obesogenic environment differentially affects the expression levels of some myomiRNAs and that this effect is modified by epicatechin.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Nanoformulation: Streamlined One-Pot Synthesis Enhances Paclitaxel Functionalization Gold Nanoparticles for Potent Anticancer Activity.","authors":"Kamini Velhal, Parvindar M Sah, Harshala S Naik, Rajesh Raut, Smitali Patil, Ramesh Yamgar, Jaya Lakkakula, Imran Uddin","doi":"10.1007/s12013-025-01701-w","DOIUrl":"https://doi.org/10.1007/s12013-025-01701-w","url":null,"abstract":"<p><p>The development of innovative, eco-friendly methods for synthesizing functional nanoparticles is crucial in advancing cancer therapeutics. This study highlights a one-pot in situ synthesis of paclitaxel-functionalized gold nanoparticles (PTX-AuNPs), with paclitaxel serving as both the reducing and stabilizing agent. The synthesis process was validated using UV-visible spectroscopy, X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, and high-resolution transmission electron microscopy (FEG-TEM). High-performance liquid chromatography (HPLC) confirmed the purity and structural integrity of paclitaxel before and after synthesis. The resulting PTX-AuNPs exhibited potent anticancer activity against human cervical cancer (SiHa) and human colon cancer (HT-29) cell lines, with a significantly stronger effect on the HT-29 cell line. A concentration-dependent reduction in HT-29 cell growth was observed as nanoparticle concentrations increased from 10 µg/mL-20 µg/mL. Molecular docking studies further demonstrated paclitaxel's strong binding affinity (-8.5 kcal/mol) to β-Tubulin, elucidating its anticancer mechanism. This cost-effective and environmentally friendly approach offers significant promise for enhancing cancer treatment strategies.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of the Oxidative Stress and ICAM-1/TLR4/NF-Κβ Levels by Metformin in Intestinal Ischemia/Reperfusion Injury in Rats.","authors":"Inci Turan, Hale Sayan Ozacmak, Veysel Haktan Ozacmak, Figen Barut","doi":"10.1007/s12013-025-01687-5","DOIUrl":"https://doi.org/10.1007/s12013-025-01687-5","url":null,"abstract":"<p><p>Metformin, a biguanide drug, is used for its antihyperglycemic effects. The purpose of the present study was to investigate the effects of metformin on the experimental model of intestinal ischemia-reperfusion (I/R) injury. Ischemia was induced by superior mesenteric artery occlusion followed by reperfusion. Metformin was administered orally by gavage at doses of 50, 100 or 200 mg/kg for one week before the surgery. Rats were divided to five groups (n = 8 for each): Sham control group; I/R control group; Metformin50 treated I/R group; Metformin100 treated I/R group; and Metformin200 treated I/R group. Tissue levels of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 (ICAM-1), toll-like receptor 4 (TLR4), and nuclear factor-κB (NF-κB) as well as histological analysis were evaluated. Metformin treatment decreased the levels of MDA in 100 and 200 mg/kg doses besides lowering the MPO activity and ICAM-1 levels in all doses. Metformin also reduced NF-κB levels at dose of 200 mg/kg and improved histopathological scores at doses of 100 and 200 mg/kg. The treatment with metformin can prevent I/R-induced intestinal injury through down-regulating ICAM-1 and NF-κB levels, reducing oxidative stress, and lowering neutrophil accumulation. We propose that metformin could be a therapeutic agent in intestinal I/R.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bromelain Protects Against PTZ-Induced Glial Damage and Inflammation: An In Vitro and In Silico Study.","authors":"Ziad Joha, Neslihan Başgöz, Aykut Özgür, Ahmet Şevki Taşkıran","doi":"10.1007/s12013-025-01703-8","DOIUrl":"https://doi.org/10.1007/s12013-025-01703-8","url":null,"abstract":"<p><p>This study aimed to investigate how bromelain protects glial cells from pentylenetetrazole (PTZ)-induced damage, focusing on its anti-inflammatory effects. C6 glioma cells were treated with PTZ, bromelain, or a combination of PTZ and bromelain. The interactions of bromelain with iNOS (Inducible Nitric Oxide Synthase) and COX2 (Cyclooxygenase-2) were investigated using molecular docking calculations. Cell viability was measured using the XTT (Methoxynitrosulfophenyl-Tetrazolium Carboxanilide) assay. iNOS, NO (Nitric Oxide), and COX2 levels were assessed using ELISA and immunofluorescence staining. Bromelain at 50 and 100 µg/mL significantly increased cell viability (p < 0.001). On the other hand, bromelain at 50 µg/mL reduced inflammation, as indicated by lower levels of NO, iNOS, and COX2 (p < 0.001). In-silico predictions suggest that bromelain can effectively target iNOS and COX2, key inflammatory proteins. These findings indicate that bromelain protects glial cells by exerting anti-inflammatory effects. However, further research is needed to understand the underlying mechanisms fully.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chaperone-Mediated Autophagy Reactivation Protects Against Severe Acute Pancreatitis-Associated Liver Injury Through Upregulating Keap1/Nrf2 Signaling Pathway and Inhibiting NLRP3 Inflammasome Activation.","authors":"Zhongbiao Li, Min Du, Jiang Wang, Xihao Zhao, Yue Qu, Dianliang Zhang","doi":"10.1007/s12013-025-01677-7","DOIUrl":"https://doi.org/10.1007/s12013-025-01677-7","url":null,"abstract":"<p><p>Acute liver injury (ALI) is a vital factor in the early progression of severe acute pancreatitis (SAP). It exacerbates systemic inflammation, impairs the liver's capacity to clear inflammatory mediators and cytokines, and contributes to systemic organ dysfunction syndrome (SODS). However, the mechanisms driving SAP-associated liver injury (SAP-ALI) are poorly understood, and effective therapeutic options remain limited. Chaperone-mediated autophagy (CMA), a selective form of autophagy, plays an essential role in reducing inflammation and oxidative stress by clearing damaged or dysfunctional proteins. This study examines the role of CMA in SAP-ALI and evaluates its therapeutic potential. In a sodium taurocholate-induced SAP-ALI rat model, CMA dysfunction was observed, characterized by reduced LAMP2A expression and the accumulation of CMA substrate proteins in pancreatic and hepatic tissues. The activator AR7 successfully restored CMA function, enhanced anti-inflammatory and antioxidant responses, and mitigated pancreatic and liver damage in SAP rat. In contrast, the CMA inhibitor PPD exacerbated liver injury, underscoring CMA's protective role in SAP-ALI. Mechanistic analyses demonstrated that CMA reactivation activated the Keap1/Nrf2 signaling pathway, leading to increased expression of antioxidant-related genes and suppression of NLRP3 inflammasome activation. Specifically, the protective effects of AR7-induced CMA activation were significantly reversed by the Nrf2 inhibitor ML385, which inhibited Nrf2 signaling and its associated protein levels. These findings show AR7-induced CMA reactivation as a promising therapeutic strategy for SAP-ALI, primarily through its enhancement of Keap1/Nrf2-regulated antioxidant pathways and inhibition of NLRP3 inflammasome activation.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of LncRNA in Pathogenesis, Diagnosis and Treatment of Chronic Kidney Disease.","authors":"Xin He, Han Li","doi":"10.1007/s12013-025-01698-2","DOIUrl":"https://doi.org/10.1007/s12013-025-01698-2","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is a clinical syndrome of metabolic disorder caused by progressive kidney impairment for more than 3 months. CKD has become a global public health problem due to its high morbidity and mortality, which is difficult to be cured for most patients. The pathogenesis of CKD is still unclear, which is closely related to glomerulosclerosis, kidney tubular injury and kidney fibrosis. LncRNA is a non-coding RNA with a length of more than 200 nucleotides. It not only participates in intracellular transcriptional regulation, post-transcriptional regulation and epigenetic activities, but also forms a regulatory network together with miRNA and mRNA, to further conduct the reticular regulation in cells. Recently, it has been found that lncRNA participates in pathophysiological mechanism of CKD by regulating glomerulosclerosis, kidney tubular injury and kidney fibrosis. This has also become a new direction of lncRNA in early diagnosis and targeted therapy of CKD.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}