Iranian Journal of Basic Medical Sciences最新文献

{"title":"Curcumin exerts protective effects against valproic acid-induced testicular damage through modulating the JAK1/STAT-3/IL-6 signaling pathway in rats.","authors":"Eda Dokumacioglu, Hatice Iskender, Kubra Asena Terim Kapakin, İSmail Bolat, Behzat Mokhtare, Ali Dogan Omur, Armagan Hayirli","doi":"10.22038/ijbms.2024.76948.16659","DOIUrl":"10.22038/ijbms.2024.76948.16659","url":null,"abstract":"<p><strong>Objectives: </strong>This experiment was carried out to investigate the protective effects of curcumin (CUR) on testicular damage induced by the valproic acid (VPA) administration.</p><p><strong>Materials and methods: </strong>Male Wistar-Albino rats (n=28, 250-300 g) were randomly divided into four groups: Control (1 ml saline, oral), VPA (500 mg/kg, IP), CUR (200 mg/kg, oral), or VPA+CUR (500 mg/kg, VPA, IP plus 200 mg/kg CUR, oral). The treatments were applied for 14 days. Serum testosterone and testis [Janus kinases1 (JAK1), signal transducers and activators of transcription-3 (STAT-3), interleukin-6 (IL-6), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-18 (IL-18), and nuclear factor (NF)-κB)] samples were collected for biochemical analyses. Semen samples were subjected to microscopy for spermatological parameters. Testis tissue was also analyzed for histopathological and immunohistochemical methods.</p><p><strong>Results: </strong>The VPA administration caused a 37% decrease in serum testosterone concentration and 5.32, 9.51, 2.44, and 3.68-fold increases in testicular tissue JAK1, STAT-3, IL-6, and MDA levels, respectively. There were also 50, 52, and 72% reductions in sperm motility, sperm viability, and the mean testicular biopsy score, respectively, accompanied by considerable degenerative changes and necrosis in seminiferous tubules in the VPA group. There is also an immune-positive reaction for IL-18 and NF-κB in only Leydig cells.</p><p><strong>Conclusion: </strong>The CUR treatment may be beneficial in restoring testicular damage through antiinflammatory and anti-oxidant potential.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"230-236"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of different pre-conditioning exercise on leptin synthesis and its downstream signalling pathway in T2DM rats.","authors":"Sen Lin, Yuzhi Hu, Shuqiao Ding, Yazhe Hu","doi":"10.22038/ijbms.2024.77774.16828","DOIUrl":"10.22038/ijbms.2024.77774.16828","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to evaluate the effects of pre-conditioning exercise on body lipid metabolism, leptin secretion, and the downstream pathways at the early stage of type 2 diabetes mellitus (T2DM).</p><p><strong>Materials and methods: </strong>The T2DM model was established using an 8-week high-sugar, high-fat diet combined. The T2DM model was established using an 8-week high-sugar, high-fat diet combined with streptozocin (STZ) injection. Two exercise interventions, high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) were performed during the model-building process. One week following the STZ injection, rats were euthanized. Blood, gastrocnemius muscle, and epididymal fat pad were collected. Plasma leptin content was measured by ELISA. The expression of leptin-mRNA in epididymal adipose tissue was measured using RT-qPCR, and its protein expression was detected by a western blot. Leptin, leptin-R, and AMPK (AMP-activated protein kinase) - ACC (Acetyl-CoA carboxylase) expression in gastrocnemius muscle was also detected by western blot. Free fatty acids (FFA) and triglycerides (TG) contents in gastrocnemius muscle were measured using a biochemical assay.</p><p><strong>Results: </strong>In the HIIT group, glucose tolerance and leptin receptor expression increased, as did the expression and phosphorylation of AMPK protein. At the early stage of T2DM, it increased significantly in the gastrocnemius muscle in the MICT group.</p><p><strong>Conclusion: </strong>At the early stage of T2DM, pre-conditioning exercise in the form of HIIT was found to inhibit the leptin-mRNA expression in adipose tissue, suppress leptin synthesis, up-regulate AMPK-ACC signaling pathway, and promote lipid decomposition in skeletal muscle tissue. Pre-conditioning of MICT led to the accumulation of FFA and TG in skeletal muscle, likely due to exercise adaptation rather than ectopic deposition of lipids.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"31-37"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Infiltration of innate and adoptive lymphoid cells in 4T1 and MC4-L2 breast cancer models.","authors":"Reihane Rasooli Tehrani, Hossein Asgarian-Omran, Saeid Taghiloo, Reza Valadan, Soheil Azizi, Abolghasem Ajami","doi":"10.22038/ijbms.2024.80535.17434","DOIUrl":"10.22038/ijbms.2024.80535.17434","url":null,"abstract":"<p><strong>Objectives: </strong>Innate lymphoid cells (ILCs) are tissue-resident lymphocytes that have vital roles in activating further immune responses. However, due to their tumor-induced diversity, we decided to examine ILCs, T cells, and the associated cytokines in mouse models of breast cancer.</p><p><strong>Materials and methods: </strong>4T1 and MC4-L2 cells were used to induce triple-negative and hormone-receptor-positive breast cancer, respectively. Tumor tissue was resected at early and late stages of tumor growth and used for further analysis. Total RNA was extracted and used in Real-Time PCR to analyze the expression of IFN-γ, IL-4, IL-10, IL-13, and IL-22. Tumor tissue was digested and used in a flow cytometric assay. H&E staining was used to examine the pathology of tumor progression.</p><p><strong>Results: </strong>Both tumor models showed a notable increase in T-cell frequency at the early stage of tumor growth. However, as the tumors progressed, the frequency of T cells significantly decreased, while the ILC component exhibited a significant increase in tumor progression. Gene analysis indicated a significant increase in the inflammatory to anti-inflammatory cytokine ratio during tumor progression in the tumor model. In contrast, this ratio was considerably reduced in advanced MC4-L2 tumors. Both tumor models showed the development of invasive breast carcinoma and lung metastasis in advanced tumors.</p><p><strong>Conclusion: </strong>Our study highlighted the expansion of ILCs during tumor progression in two distinct breast cancer models with different immunogenicity. These findings suggest that ILCs may actively modulate the tumor microenvironment during the advanced stage of tumor growth.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"63-71"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoformulation innovations: Revolutionizing precision in migraine therapy.","authors":"Mohammad Ghasemi Narimani, Fatemeh Kalalinia, Somayeh Marouzi, Sara Gheshlaghi, Zahra Salmasi, Maryam Hashemi","doi":"10.22038/ijbms.2024.79824.17290","DOIUrl":"10.22038/ijbms.2024.79824.17290","url":null,"abstract":"<p><strong>Objectives: </strong>Migraine, a serious neurological disease that affects millions of people worldwide, is one of the most considerable burdens on the healthcare system and has significant economic implications. Even though various treatment methods are available, including medication, lifestyle changes, and behavioral therapy, many migraine sufferers do not receive adequate relief or experience intolerable side effects. Hence, the present review aims to evaluate the nanoformulation regarding migraine therapy.</p><p><strong>Materials and methods: </strong>Between 2005 and 2024, specific keywords were used to search several databases, such as Pubmed, Google Scholar, and Scopus.</p><p><strong>Results: </strong>The nanoformulation field is an increasing field within nanotechnology that offers new solutions for treating migraine, including improving drug delivery, increasing therapeutic efficacy, and minimizing side effects. By combining nanoscale materials with therapeutic agents, nanoformulations can enhance bioavailability, sustain drug release, deliver targeted drugs, and penetrate the Blood-Brain Barrier (BBB) more efficiently. Nanoformulation has the potential to be a useful tool for migraine therapy. However, several challenges still need to be overcome, such as the BBB penetration, safety and biocompatibility of the product, manufacturing, and scalability reproducibility to pass regulatory approval and affordability. To overcome these challenges, research efforts should be focused on developing innovative techniques to penetrate the BBB, target specific migraine pathways, incorporate personalized medicine approaches, and develop nanotechnology-based diagnostics.</p><p><strong>Conclusion: </strong>A nanotechnology-based approach aims to revolutionize migraine therapy, improving patient outcomes and living standards by offering personalized and precise treatments.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"16-30"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of VDAC1 in hepatocyte apoptosis during acute liver injury in rats induced by obstructive jaundice.","authors":"Jinshan Liu, Jinlong Hu, Hongyu Xu, Liang Yan, Jiaming Yao, Baoqiang Cao","doi":"10.22038/ijbms.2024.78454.16962","DOIUrl":"10.22038/ijbms.2024.78454.16962","url":null,"abstract":"<p><strong>Objectives: </strong>Exploring the role of VDAC1 in hepatocyte apoptosis during acute liver injury induced by obstructive jaundice.</p><p><strong>Materials and methods: </strong>Animal and cell models were established to investigate possible mechanisms during acute liver injury induced by OJ. Blood was collected for liver function assessment. H&E and TEM were employed to observe pathological changes in the liver tissues. Flow cytometry was used to measure the hepatocyte apoptosis. The mitochondrial MPTP assay was employed to assess the mitochondrial function of hepatocytes. IHC, western blot, and qRT-PCR were employed to determine the expression levels of VDAC1. Then, VDAC-siRNA was used to establish a knockdown model. Flow cytometry was used again to measure hepatocyte apoptosis following VDAC1 knockdown.</p><p><strong>Results: </strong>The serum of rats in the OJ group exhibited a significant increase in liver function. Irregular tissue structure and mitochondrial morphology were observed in the liver tissues of OJ rats. A significant increase in mitochondrial permeability in hepatocytes. The expression levels of VDAC1 were significantly increased in the liver tissue of OJ rats. They were also significantly increased in the hepatocytes, primarily within mitochondrial membranes, determined by western blot <i>in vivo</i> and <i>in vitro</i>. Significant increases in the rates of hepatocyte apoptosis, particularly early apoptosis, were observed in the OJ groups. However, there was a reverse in the rates of hepatocyte apoptosis after knockdown regulation of VDAC1 only within the cells of the OJ group.</p><p><strong>Conclusion: </strong>The up-regulation of VDAC in liver injury caused by obstructive jaundice may lead to increased early apoptosis of hepatocytes.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"87-97"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COTI-2 suppresses the malignancy of bladder cancer by inducing apoptosis via the AMPK-mTOR signaling pathway.","authors":"Yuancai Zheng, Keqi Wang, Chenyu Wu, Yuying Qin, Yihan Sun, Xinyu Lu, Yupeng Xu, Gonghui Li","doi":"10.22038/ijbms.2024.80284.17378","DOIUrl":"10.22038/ijbms.2024.80284.17378","url":null,"abstract":"<p><strong>Objectives: </strong>COTI-2, an innovative oral homocysteine, has shown promising antitumor results on multiple types of cancer. However, its effects in treating bladder cancer (BCa) and the underlying molecular mechanisms have not been elucidated. The present study aimed to explore the antitumor effects of COTI-2 on BCa and the potential mechanisms.</p><p><strong>Materials and methods: </strong>BCa cell lines, including the 5637 and T24 cell lines, were treated with COTI-2 at concentrations of 0.5 and 1 μM, respectively. Cell Counting Kit (CCK)-8 assay, colony formation assay, apoptosis assay, and transwell migration and invasion assay were conducted to evaluate the antitumor effects of COTI-2 on BCa cells. Western blotting, H&E, immunohistochemical staining, and immunofluorescence analysis were performed to investigate the underlying mechanisms. Moreover, a xenograft model in nude mice using T24 cells was generated to determine the antitumor activities of COTI-2 <i>in vivo</i>.</p><p><strong>Results: </strong>COTI-2 highly inhibited the proliferation of BCa cell lines, including 5637 and T24 cells, and induced their apoptosis. Moreover, it efficiently suppressed the migration and invasion of BCa cells. Additionally, the subcutaneous xenograft model in nude mice showed that COTI-2 treatment inhibited the tumor growth of BCa by inducing its apoptosis in vivo. We also found that COTI-2 promoted apoptosis in BCa cells, presumably through activating the AMPK/mTOR pathway.</p><p><strong>Conclusion: </strong>Our data suggest that COTI-2 effectively reduces the malignancy of BCa, probably by inducing apoptosis via the AMPK/mTOR signaling pathway. These data highlight the potential of COTI-2 as a therapeutic agent for the treatment of BCa.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"240-246"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plinabulin exerts an anti-proliferative effect via the PI3K/AKT/mTOR signaling pathways in glioblastoma.","authors":"Rouxin Wang, Jing Cheng, Huanqi Zhang, Kaizhi Luo, Rui Wu, Yangling Li, Yuanheng Zhu, Chong Zhang","doi":"10.22038/ijbms.2024.79406.17200","DOIUrl":"10.22038/ijbms.2024.79406.17200","url":null,"abstract":"<p><strong>Objectives: </strong>Plinabulin, a marine-derived anticancer drug targeting microtubules, exhibits anti-cancer effects on glioblastoma cells. However, its therapeutic potential, specifically for glioblastoma treatment, remains underexplored. This study aims to elucidate the mechanisms by which plinabulin exerts its effects on glioblastoma cells.</p><p><strong>Materials and methods: </strong>Using the SRB and colony formation assay to observe the effect of plinabulin on glioblastoma cell viability. Wound healing and transwell migration assay were used to test the effect of plinabulin on glioblastoma cell metastatic potential. Crucial target genes were identified through RNA sequencing and bioinformatics analysis. Protein levels were evaluated in a concentration-dependent manner using western blot analysis.</p><p><strong>Results: </strong>Plinabulin suppressed glioblastoma cell proliferation by causing cell cycle G2/M phase arrest and inhibited migration. The IC50 values were 22.20 nM in A172 cells and 20.55 nM in T98G cells. Plinabulin reduced AKT and mTOR phosphorylation. Combined with the AKT/mTOR inhibitors LY294002 and rapamycin, plinabulin decreased p-mTOR and EGFR protein levels and increased cleaved-PARP levels. Plinabulin induces autophagy, and using an autophagy inhibitor enhances plinabulin-induced cell apoptosis. This suggests that plinabulin might trigger cytoprotective autophagy in glioblastoma cells. These findings indicate that plinabulin hinders glioblastoma growth and induces protective autophagy via the PI3K/AKT/mTOR pathway. Additionally, plinabulin combined with erlotinib showed greater cytotoxic efficacy than either drug alone in glioblastoma cells <i>in vitro</i>.</p><p><strong>Conclusion: </strong>Our study provides new insights into the efficacy of plinabulin against glioblastoma and highlights the potential clinical utility of combining plinabulin with EGFR inhibitors as a chemotherapy strategy.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"113-120"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of <i>Lavandula angustifolia</i> essential oil inhalation on neuromodulators regulating the sleep/wake cycle in rats with total sleep deprivation.","authors":"Arzu Yalcin, Mustafa Saygin, Ozlem Ozmen, Rahime Aslankoc, Önder Özturk, Hasan Aslancan, Oguzhan Kavrik","doi":"10.22038/ijbms.2024.78085.16880","DOIUrl":"10.22038/ijbms.2024.78085.16880","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to investigate the potential effects of different doses of <i>Lavender angustifolia</i> essential oil (Lavender EO) administered by inhalation on sleep latency and neuromodulators regulating the sleep/wake cycle in rats with total sleep deprivation (TSD).</p><p><strong>Materials and methods: </strong>Forty-eight male Sprague-Dawley rats were divided into five groups: Control, Alprazolam (ALP, 0.25 mg/kg given intraperitoneally), L1 (Lavender EO, 0.3 ml given by inhalation), L2 (Lavender EO, 0.5 ml given by inhalation), and L3 (Lavender EO, 1 ml given by inhalation); TSD was applied to all groups. Rats in SD groups were kept on a platform surrounded by water for 18 hr for 20 days, and for the remaining time, the animals were exposed to Lavender EO for 1 hr (11:00-12:00) and then were kept in their home cage for 5 hr (12:00-17:00). Their brain and brainstem were removed for histopathological and immunohistochemical analyses (c-Fos, ChAT, GAD, and ADRB2 expression) in the locus coeruleus (LC), basal forebrain (BF), and preoptic area (PO).</p><p><strong>Results: </strong>The groups ranked by the severity of edema, hyperemia, and neurodegeneration in LC, BF, and PO areas were control, L3, L1, L2, and ALP. c-Fos expression significantly decreased in all brain regions in all groups except the L1 group. ChAT and GAD expressions increased dramatically in all brain regions. ADRB2 significantly increased in LC in ALP and L2 groups; in the PO area in ALP, L1, and L2 groups; and in BF in all groups.</p><p><strong>Conclusion: </strong>Lavender EO treatment ameliorated c-Fos, ChAT, GAD, and ADRB2 expression, similar to the effect of ALP.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"264-272"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydroxytyrosol protects isoproterenol-induced myocardial infarction through activating notch signaling.","authors":"Elif Onat, Ahmet Türk, Nevin Kocaman, Serhat Hançer, Solmaz Susam, Ali Parlar, Selin Turhan, Mehmet Kaya Özer","doi":"10.22038/ijbms.2024.81495.17637","DOIUrl":"10.22038/ijbms.2024.81495.17637","url":null,"abstract":"<p><strong>Objectives: </strong>In this investigation, the protective effects of hydroxytyrosol (HT) administered prior to myocardial infarction in rats were examined, with a particular focus on its potential roles within the Notch pathway.</p><p><strong>Materials and methods: </strong>The animals were categorized into seven groups (n=7): control, myocardial infarction (MI) 6^th hr, MI 24^th hr, MI 7^th day, MI+HT 6^th hr, MI+HT 24^th hr, MI+HT 7^th day. In order to create infarction, the rats received a subcutaneous injection of isoproterenol at a dose of 200 mg/kg. Rats were given 4 ml/kg/day liquid containing HT orally for six weeks before infarction. Histopathological examination was conducted on heart tissue to assess Notch1, Hes1, and DLL4. Biochemical parameters were analyzed in serum using the ELISA method.</p><p><strong>Results: </strong>The study revealed an increase in Notch1 and DLL4 levels, particularly at the 24^th hr and 7^th day after the occurrence of myocardial infarction. DLL4 increased at 24 hr and 7 days of infarction after HT administration compared to control. Hes1 levels increased towards the seventh day after infarction and following HT application before infarction. It was noted that the severity of histopathological damage in heart tissue was reduced at the 24^th hr of infarction in rats treated with HT prior to infarction. A significant decrease in fibrosis was observed on the seventh day of infarction in rats given HT before infarction. The levels of biochemical parameters decreased with the administration of HT before the occurrence of infarction.</p><p><strong>Conclusion: </strong>HT is thought to exert a cardioprotective effect in MI, potentially mediated through the Notch pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"217-223"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of pentoxifylline on mouse oocytes maturation and quality <i>in vitro</i>.","authors":"Junjiao Wu, Jianbo Wu, Yanyan Xu","doi":"10.22038/ijbms.2024.77926.16856","DOIUrl":"10.22038/ijbms.2024.77926.16856","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the impact of Pentoxifylline (PTX) on the <i>in vitro</i> maturation (IVM) of mouse oocytes and its effect on oocyte quality.</p><p><strong>Materials and methods: </strong>This experimental study involved culturing mouse oocytes in an IVM medium with varying PTX concentrations (0-100 μM). Post-culture, oocytes were assessed for nuclear and cytoplasmic maturation and quality indicators, including germinal vesicle breakdown (GVBD), first polar body extrusion (PB1E), cortical granules (CGs) distribution, spindle structure, chromosome alignment, and intracellular reactive oxygen species (ROS) levels.</p><p><strong>Results: </strong>Treatment with PTX at 10, 25, and 50 μM concentrations significantly enhanced the nuclear maturation rates of oocytes. The optimal concentration was found to be 10 μM, as it resulted in the most favorable cytoplasmic maturation, characterized by improved distribution of CGs, spindle structure, and chromosome alignment. Additionally, treatment with 10 μM PTX effectively reduced reactive oxygen species (ROS) levels.</p><p><strong>Conclusion: </strong>PTX supplementation at specific concentrations enhances mouse oocyte maturation and quality, potentially by facilitating CG distribution, spindle integrity, and chromosome alignment and by reducing ROS production.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"310-315"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}