{"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}
Mohammad Ghasemi Narimani, Fatemeh Kalalinia, Somayeh Marouzi, Sara Gheshlaghi, Zahra Salmasi, Maryam Hashemi
{"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}
Sara Mostafalou, Fatemeh Moafi-Madani, Maryam Baeeri, Mahban Rahimifard, Hamed Haghi-Aminjan
{"title":"Azelaic acid reduces arsenic-induced toxicity and inflammation in the rat islets of langerhans.","authors":"Sara Mostafalou, Fatemeh Moafi-Madani, Maryam Baeeri, Mahban Rahimifard, Hamed Haghi-Aminjan","doi":"10.22038/ijbms.2025.84651.18311","DOIUrl":"https://doi.org/10.22038/ijbms.2025.84651.18311","url":null,"abstract":"<p><strong>Objectives: </strong>Arsenic is classified as a toxic metal that is naturally found in the Earth's crust, and long-term exposure to it can result in chronic human disorders like cancer and diabetes. Azelaic acid (AZA), a natural dicarboxylic acid, has been reported to have anti-oxidant and anti-inflammatory effects; hence, it may protect against the metabolic toxicity of arsenic. This study aimed to investigate whether AZA could ameliorate sodium arsenite (SA) toxicity toward rat islets of Langerhans.</p><p><strong>Materials and methods: </strong>Pancreatic Islets of Langerhans isolated from adult male Wistar rats were divided into four groups of 10: control, SA, AZA, and SA plus AZA. Twenty-four hours after incubation, cell viability, cell death pathways, reactive oxygen species (ROS), inflammatory factor gene expression, and insulin secretion were evaluated.</p><p><strong>Results: </strong>SA dose-dependently decreased cell viability, increased apoptosis, ROS generation, expression of inflammatory mediators (NF-κB, IL-1β, and TNF-α), and insulin secretion. AZA was able to ameliorate all these changes significantly.</p><p><strong>Conclusion: </strong>Our results indicate that SA can potentially disrupt cellular homeostasis and function in the islets of Langerhans and can increase the risk of metabolic diseases such as diabetes. On the other hand, AZA protected islets of Langerhans against the toxic effects of SA, seemingly due to its anti-apoptotic, anti-inflammatory, and anti-oxidant properties, indicating that AZA may have the potential to run intracellular mechanisms beneficial for coping with the metabolic toxicity of arsenic.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"784-789"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009519","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}
Elif Onat, Ahmet Türk, Nevin Kocaman, Serhat Hançer, Solmaz Susam, Ali Parlar, Selin Turhan, Mehmet Kaya Özer
{"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<sup>th</sup> hr, MI 24<sup>th</sup> hr, MI 7<sup>th</sup> day, MI+HT 6<sup>th</sup> hr, MI+HT 24<sup>th</sup> hr, MI+HT 7<sup>th</sup> 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<sup>th</sup> hr and 7<sup>th</sup> 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<sup>th</sup> 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}
Arzu Yalcin, Mustafa Saygin, Ozlem Ozmen, Rahime Aslankoc, Önder Özturk, Hasan Aslancan, Oguzhan Kavrik
{"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":"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}
Fatemeh Forouzanfar, Ali Mohammad Pourbagher-Shahri, Amir Mahmoud Ahmadzadeh
{"title":"Rutin attenuates complete Freund's adjuvant-induced inflammatory pain in rats.","authors":"Fatemeh Forouzanfar, Ali Mohammad Pourbagher-Shahri, Amir Mahmoud Ahmadzadeh","doi":"10.22038/ijbms.2024.81572.17655","DOIUrl":"10.22038/ijbms.2024.81572.17655","url":null,"abstract":"<p><strong>Objectives: </strong>Rutin is a bioflavonoid compound renowned for its anti-oxidative, anti-inflammatory, and antinociceptive properties. The present study aims to assess its therapeutic efficacy on complete Freund's adjuvant (CFA)induced inflammatory pain.</p><p><strong>Materials and methods: </strong>Arthritis was induced in Wistar rats via subcutaneous administration of CFA into the right hind paw. Rutin (15 and 30 mg/kg) and indomethacin (5 mg/kg, orally) were given once daily for three weeks. Parameters observed included alterations in paw swelling perimeter, arthritis scores, and body weight. Additionally, antinociceptive activity was measured through thermal hyperalgesia and cold allodynia responses. The Tumor necrosis factor-alpha (TNF-α) level in the serum was measured. Malondialdehyde (MDA), thiol levels, catalase, and superoxide dismutase (SOD) activities were also evaluated as serum oxidative stress markers.</p><p><strong>Results: </strong>Rutin and indomethacin significantly suppressed alterations in paw edema, pain responses, and arthritis scores and reduced the loss of body weight in contrast to disease-control rats. Furthermore, in contrast to disease control rats, rutin and indomethacin treatment exhibited an anti-inflammatory effect through a marked reduction in TNF-α levels in the serum. Rutin and indomethacin demonstrated a significant increase in catalase and SOD activities, a total thiol level, and a decrease in MDA level compared to the disease-control rats.</p><p><strong>Conclusion: </strong>These results suggest that rutin's antiarthritic effect is mediated by its antinociceptive, anti-oxidant, and anti-inflammatory properties.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"332-339"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189087","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":"Rosmarinic acid attenuated inflammation and apoptosis in folic acid-induced renal injury: Role of FoxO3/ NFκB pathway.","authors":"Maryam Mottaghi, Fatemeh Heidari, Tahereh Komeili Movahed, Akram Eidi, Azam Moslehi","doi":"10.22038/ijbms.2024.80551.17436","DOIUrl":"10.22038/ijbms.2024.80551.17436","url":null,"abstract":"<p><strong>Objectives: </strong>Rosmarinic acid (RA) is a herbal compound with various antioxidant and anti-inflammatory effects. This study aimed to explore the anti-inflammatory and anti-apoptotic properties of RA in folic acid-induced renal injury.</p><p><strong>Materials and methods: </strong>Thirty-six male C57/BL6 mice were randomly divided into six groups (N=6): Control (received normal saline), NaHCO<sub>3</sub> (received NaHCO<sub>3</sub> as folic acid solvent), FA (received folic acid (FA)(IP) to induce renal injury), RA (received 100 mg/kg RA), RA50-FA (received 50 mg/kg RA solution after folic acid injection), and RA100-FA (received 100 mg/kg RA after folic acid injection). For ten days, the treatment groups received RA by gavage. The effects of RA were assessed using H & E staining, biochemical tests, western blotting, and ELISA in the kidney tissues of the mice. Real-time RT-PCR was also performed to evaluate the expression changes of renal genes.</p><p><strong>Results: </strong>Our data showed that treatment by RA led to the over-expression of FoxO3 (<i>P</i><0.05) and decrease in NFκB levels (<i>P</i><0.01 and <i>P</i><0.05) and expression of TNFα (<i>P</i><0.05) and IL6 (<i>P</i><0.001 and <i>P</i><0.01). Other evaluations showed a decrease in p53 (<i>P</i><0.01 and <i>P</i><0.001), Bax/Bcl-2 ratio expression (<i>P</i><0.01 and <i>P</i><0.05), and Caspase-3 level (<i>P</i><0.01 and <i>P</i><0.05) compared to the folic acid group. Histological and biochemical results also confirmed the attenuation of tissue damage.</p><p><strong>Conclusion: </strong>This study revealed that RA's positive effects on folic acid-induced renal injury might result from the involvement of the FoxO3/NFκB pathway, thereby suppressing inflammation and apoptosis.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"316-322"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189140","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":"Salidroside impedes Ang II-infused myocardial fibrosis by activating the SIRT1-Nrf2 pathway.","authors":"Xi Zhu, Zhen Hai, Zhongping Ning","doi":"10.22038/ijbms.2025.83659.18105","DOIUrl":"https://doi.org/10.22038/ijbms.2025.83659.18105","url":null,"abstract":"<p><strong>Objectives: </strong>This research examined the protective function of salidroside (SAL) against angiotensin II (Ang II)-infused myocardial fibrosis and its associated mechanism.</p><p><strong>Materials and methods: </strong>The C57BL/6 male murine models (n=24) received either saline solution or Ang II (1500 ng/kg/day) subcutaneously and an oral dosage of SAL (50 mg/kg/day) once daily for 28 days. Newborn Sprague-Dawley (SD) rats were used to isolate atrial fibroblasts.</p><p><strong>Results: </strong>The fibrotic region was raised by Ang II infusion, while SAL treatment inhibited it. Collagen I and III expression was raised by Ang II induction, but SAL therapy reduced their expression. SAL therapy also decreased the expression of other fibroblast differentiation-related markers induced by Ang II infusion. It elevated SIRT1, Nrf2, and HO-1 levels in atrial fibroblasts. Additionally, SAL significantly inhibited atrial fibroblasts, whereas EX527, an inhibitor of SIRT1, noticeably increased the migration ability. Furthermore, SAL suppressed intracellular ROS production and oxidative stress in Ang II-infused atrial fibroblasts.</p><p><strong>Conclusion: </strong>SAL protects against myocardial fibrosis infused by Ang II by activating the SIRT1-Nrf2 pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"815-824"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990722","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}