Iranian Journal of Basic Medical Sciences最新文献

{"title":"Echinacoside alleviates Ang II-induced cardiac fibrosis by enhancing the SIRT1/IL-11 pathway.","authors":"Yingbiao Wu, Zhongping Ning","doi":"10.22038/ijbms.2024.79837.17296","DOIUrl":"10.22038/ijbms.2024.79837.17296","url":null,"abstract":"<p><strong>Objectives: </strong>Echinacoside (ECH) is an anti-fibrotic phenylethanoid glycoside derived from the <i>Cistanche</i> plant that protects against cardiac dysfunction by mitigating apoptosis, oxidative stress, and fibrosis. Nevertheless, ECH's precise function and mechanisms in addressing cardiac fibrosis are still not fully understood.</p><p><strong>Materials and methods: </strong>In our current investigation, we induced cardiac fibrosis in mice by administering Angiotensin II (Ang II) and subsequently assessed the effects of ECH treatment four weeks post-fibrosis induction. Additionally, in an <i>in vitro</i> setting, we exposed cardiac fibroblasts (CFs) to Ang II to prove the anti-fibrotic mechanisms of ECH.</p><p><strong>Results: </strong>ECH treatment effectively reversed cardiac fibrosis in the mice model. ECH treatment significantly reduced the levels of fibrosis-related genes, such as α-SMA, Collagen I, and Collagen III (all, <i>P<</i>0.001). Moreover, it reduced the number of apoptotic cells and regulated the expression of apoptosis-related genes, such as BAX and BCL-2 (all, <i>P<</i>0.001). ECH treatment also positively affected serum levels of markers associated with cardiac fibrosis, including LDH, CK-MB, ANP, BNP, CTnl, and CTnT (all, <i>P<</i>0.001), in the <i>in vivo</i> experiments. In the <i>in vitro</i> studies, ECH pretreatment alleviated cardiac fibroblast apoptosis and reduced cell migration, collagen deposition, and MMP expression (all, <i>P<</i>0.001). In our <i>in vivo</i> and <i>in vitro</i> investigations, we observed that ECH treatment reversed the down-regulation of SIRT1 and up-regulation of IL-11 following cardiac fibrosis. The results suggest that the protective effects of ECH may involve regulating the SIRT1/IL-11 pathway.</p><p><strong>Conclusion: </strong>ECH may protect against Ang II-induced cardiac fibrosis via the SIRT1/IL-11 pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"130-139"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058977","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":"Comparing the effect of plasma therapy with estradiol valerate in motor and cognitive behavioral disorders in ovariectomized old rats: Behavioral, biochemical, and protein expression.","authors":"Maryam Khajvand-Abedini, Mohammad Mohammadi, Parisa Habibi, Zahra Shahabi, Siamak Shahidi, Nasser Ahmadiasl, Mohammad Reza Alipour, Mahdi Ramezani, Alireza Komaki","doi":"10.22038/ijbms.2024.81345.17608","DOIUrl":"10.22038/ijbms.2024.81345.17608","url":null,"abstract":"<p><strong>Objectives: </strong>This study investigated the effects of young plasma therapy (YPT) compared to estrogen therapy (E2T) on motor and cognitive impairments in aged ovariectomized (OVX) rats.</p><p><strong>Materials and methods: </strong>Sixty female Wistar rats were divided as follows: 1). 2-3 months control young group. Five 22-24 months old groups: 1) Control, 2) Sham, 3) OVX, 4) OVX.E2, and 5) OVX.YP. Young plasma (1 ml plasma, through the tail vein, 3 days weekly for 4 weeks) and E2 (30 mg/kg, SC, 5 days weekly for 4 weeks) were administrated to OVX rats. The open field, elevated plus maze, and Barne's maze were used to assess the behaviors. Then, miR-134 and miR-124 (RT- RCR), SIRT1, CREB, and BDNF (western blot), and anti-oxidants/oxidants markers (Photometry) levels were assessed in the rat's hippocampal tissues.</p><p><strong>Results: </strong>OVX caused up-regulated hippocampal miR-134 and miR-124 expression levels (<i>P</i><0.001) while down-regulated SIRT1, CREB, and BDNF protein expressions (<i>P</i><0.001). Also, ovariectomy Increased TOS, OSI, and MDA (<i>P</i><0.001) while decreasing TAC (<i>P</i><0.001) compared to sham. Treatment with both E2T and YPT significantly improved all oxidative stress indexes (<i>P</i><0.0.001) and increased p-CREB, BDNF, and SIRT1 protein levels (<i>P</i><0.05, <i>P</i><0.01) while decreasing the expression of miR-134 and miR-124 (<i>P</i><0.001).</p><p><strong>Conclusion: </strong>YPT is a non-pharmacological therapeutic as much as or more than E-2T, which can exhibit anti-oxidative and anti-inflammatory potential in the hippocampal tissue and improve cognitive deficits in aged OVX rats without unknown side effects.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"366-375"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188011","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 the amygdala opioid system in the effects of stress on the post-learning sleep patterns of male Wistar rats.","authors":"Mehdi Graily-Afra, Farideh Bahrami, Zahra Bahari, Hedayat Sahraei, Zeinab Shankayi, Ali Gharib","doi":"10.22038/ijbms.2024.79291.17266","DOIUrl":"10.22038/ijbms.2024.79291.17266","url":null,"abstract":"<p><strong>Objectives: </strong>Three physiological processes interact: sleep, learning, and stress. It is essential to understand how stress affects and interacts with the link between sleep, learning, and memory since it has long been recognized that sleep plays a crucial role in memory consolidation and learning. Through naloxone injection in the baso lateral amygdala (BLA), this study intends to shed light on the interactions between stress, learning, and sleep, as well as the function of the opioid system and its impact on brain-derived neurotrophic factor (BDNF) production in the hippocampus.</p><p><strong>Materials and methods: </strong>Male Wistar rats (n=77) in eleven groups were implanted with electroencephalogram (EEG) and electromyography (EMG) recording electrodes, and the BLA area was bilaterally cannulated. Recordings of Rapid Eye Movement (REM) and Non-Rapid Eye Movement (NREM) sleep and wakefulness steps were made for the three hours prior to and three hours following the implementation of the immobility stress protocol and learning with the Barnes maze for three consecutive days. Also, the animals' memory was tasted 48 hr later. Before the stress and learning procedure, naloxone was injected into each BLA three times in a row at a dosage of 0.05 μg or 0.1 μg in a volume of 0.5 μl. A molecular biomarker of learning and stress, BDNF, was also examined.</p><p><strong>Results: </strong>The study demonstrated that the immobility stress model lowers REM and NREM sleep. On the other hand, putting the learning technique into practice results in more REM and NREM sleep, and stress situations do not stop this rise after learning. Naloxone injections in the BLA region also enhance learning and memory, preventing stress-related REM and NREM sleep loss. Additionally, stress lowers BDNF expression in the hippocampal region. BDNF expression rises in the hippocampus throughout the learning process, and naloxone administration in the BLA area also raises BDNF expression in the hippocampus.</p><p><strong>Conclusion: </strong>Stress generally reduces REM, NREM, and BDNF expression in the hippocampal region. Under stress, using the learning protocol increases REM, NREM sleep, and BDNF. Naloxone injection in BLA improves memory and learning, reducing stress-induced memory loss.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"283-291"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189024","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":"Synergistic effect of cold atmospheric plasma and methylene blue loaded nano micelles on treating human glioblastoma cells: An in vitro and molecular dynamics study.","authors":"Elahe Ahmadi, Armin Imanparast, Mehdi Hoseini, Shahrokh Naseri, Samaneh Soudmand Salarabadi, Ameneh Sazgarnia","doi":"10.22038/ijbms.2024.79858.17304","DOIUrl":"10.22038/ijbms.2024.79858.17304","url":null,"abstract":"<p><strong>Objectives: </strong>One of the most recent cancer treatment methods is cold atmospheric plasma (CAP), which destroys cancer cells without affecting healthy cells. Also, the created photons in the CAP flame can be used to excite a proper photosensitizing agent (PS). Therefore, using nano micelle systems containing a proper photosensitizer may be beneficial in raising the treatment efficacy of CAP. In this study, we utilized molecular dynamics (MD) simulation to optimize a nano micellar system containing methylene blue to take advantage of the induced photodynamic effect of a CAP generator with helium gas on a glioblastoma cell line.</p><p><strong>Materials and methods: </strong>Some micelle properties were first determined and optimized by MD with GROMACS software. Then, micelles containing methylene blue (Micelle-MB) and free methylene blue (MB) at various concentrations were prepared. Singlet oxygen dosimetry using 1,3-diphenylisobenzofuran (DPBF)was performed in the presence and absence of Micelle-MB and MB. Subsequently, the cytotoxicity of MB and Micelle-MB was evaluated on U87-MG cancer cells, and their half-maximal inhibitory concentrations (IC₅₀) were determined. After 48 hr of treatment, the percentage of cell survival was determined using the MTT test. The experiments were repeated at least three times. The synergy index was selected to compare the results.</p><p><strong>Results: </strong>Treatment with CAP and MB reduced the survival rate compared to the PS-free group with CAP. Results of singlet oxygen dosimetry showed that Micelle-MB might be more efficient in producing ROS. CAP treatment with Micelle-MB resulted in more cell death than free MB. In addition, cell viability decreased in Micelle-MB groups with increasing irradiation time in the three investigated irradiation times.</p><p><strong>Conclusion: </strong>Using Micelle-MB in the CAP treatment improves treatment efficiency in the U87-MG cell line.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"299-309"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189094","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":"Sulforaphane alleviates membranous nephropathy by inhibiting oxidative stress-associated podocyte pyroptosis.","authors":"Daoyuan Lv, Laping Chu, Yuan Du, Chunqing Li, Neng Bao, Yuqing Su, Gang Wang, Yanlie Zheng, Yafen Yu","doi":"10.22038/ijbms.2024.78960.17083","DOIUrl":"10.22038/ijbms.2024.78960.17083","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the natural product sulforaphane (SFN) in protection of membranous nephropathy (MN) by inhibiting oxidative stress-associated podocyte pyroptosis.</p><p><strong>Materials and methods: </strong>A passive Heymann nephritis (PHN) model was established and treated with SFN. Clinical manifestations were examined by testing 24-hr urine protein, albumin, total cholesterol, triglyceride, high-density and low-density lipoprotein levels. Podocyte injury was observed through glomerular ultrastructure and the expression of podocin and desmin. Intrarenal oxidative stress was evaluated through assessment of oxidative markers, including malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine, and the activities of anti-oxidant enzymes, including total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. Podocyte and intrarenal pyroptosis were investigated by observing the localization of the GSDMD N-terminus (GSDMD(N)) in podocytes; the expression of pyroptosis signaling pathway, including GSDMD, NF-κB p65, p-NF-κB p65 (Ser536), NLRP3, ASC, caspase-1, IL-1β, and IL-18; and pyroptosis encounter Nrf2 in the glomeruli and kidney.</p><p><strong>Results: </strong>SFN has a protective effect on MN, as reflected by alleviation of nephrotic syndrome, amelioration of podocyte foot process fusion, increased expression and normalization of podocin, and decreased expression of desmin in the glomeruli. Mechanistically, SFN relieved intrarenal oxidative stress, as indicated by decreased renal malondialdehyde, 8-isoprostane, and 8-hydroxydeoxyguanosine and increased activity of total superoxide dismutase, catalase, and γ-glutamylcysteine synthetase. SFN also inhibited podocyte and intrarenal pyroptosis, as revealed by decreased colocalization of GSDMD (N) with synaptopodin and ZO-1, decreased expression of pyroptosis signaling pathway, and increased expression of Nrf2 in the glomeruli and kidney.</p><p><strong>Conclusion: </strong>SFN could alleviate MN by inhibiting oxidative stress-associated podocyte pyroptosis.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"237-244"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028713","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":"Effect of the S100A9/AMPK pathway on PM2.5-mediated mouse lung injury.","authors":"Yunxia Li, Yuxin Bai, Shiyu Tang, Ye Sun, Zhe Wang, Biao Yang, Guangyan Liu","doi":"10.22038/ijbms.2024.80242.17374","DOIUrl":"10.22038/ijbms.2024.80242.17374","url":null,"abstract":"<p><strong>Objectives: </strong>Particulate matter 2.5 (PM2.5), particles with an aerodynamic diameter less than 2.5 µm, affect lung function and increase respiratory disease incidence and mortality rate. The molecular mechanism of lung injury and epithelial damage after PM2.5 exposure is not completely clear.</p><p><strong>Materials and methods: </strong>Mouth-nose exposure of mice was performed with PM2.5 or neutral saline. <i>In vitro</i> experiments were conducted to investigate the role of the S100A9/AMPK pathway in PM2.5-mediated lung injury.</p><p><strong>Results: </strong>PM2.5 exposure in mice caused lung epithelial damage, alveolar wall thickening, and alveolar wall structure destruction. The 16S rRNA sequencing results suggested that the microecology structure of lung tissue was altered after PM2.5 exposure. Proteomic sequencing was performed to explore the underlying mechanism, and 71 differentially expressed proteins were identified. KEGG database analysis of the up-regulated differential proteins revealed regulatory networks, including fat digestion and absorption, the AMPK signaling pathway, and the PPAR signaling pathway. Moreover, PM2.5 exposure in mice increased the level of S100A9 and ROS, leading to reduction of the ATP level. To achieve a sufficient energy supply by increasing fatty acid transfer and oxidation, activated AMPK up-regulates CD36 and CPT1, which leads to mitochondrial damage of PM2.5-exposed cells and injury or death of lung epithelial cells. siRNA-S100A9 and AMPK inhibitors significantly reduced the occurrence of cell damage.</p><p><strong>Conclusion: </strong>These results may help to clarify biomarkers and specific mechanisms of lung tissue injury induced by PM2.5 exposure.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"121-129"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058982","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 combo therapy with coenzyme Q10 and mitochondrial transplantation on myocardial ischemia/reperfusion-induced arrhythmias in aged rats.","authors":"Soleyman Bafadam, Behnaz Mokhtari, Alireza Alihemmati, Reza Badalzadeh","doi":"10.22038/ijbms.2024.80092.17348","DOIUrl":"10.22038/ijbms.2024.80092.17348","url":null,"abstract":"<p><strong>Objectives: </strong>Ischemia/reperfusion (IR)-induced ventricular arrhythmia, which mainly occurs after the opening of coronary artery occlusion, poses a clinical problem. This study aims to investigate the effectiveness of pretreatment with coenzyme Q₁₀ (CoQ₁₀) in combination with mitochondrial transplantation on IR-induced ventricular arrhythmias in aged rats.</p><p><strong>Materials and methods: </strong>Myocardial IR induction was performed by left anterior descending coronary artery occlusion for 30 min, followed by re-opening for 24 hr. CoQ₁₀ was administered intraperitoneally at a dosage of 10 mg/kg/day for two weeks before inducing IR. At the start of reperfusion, 500 µl of the respiration buffer containing 6×10⁶±5×10⁵ mitochondria/ml of respiration buffer harvested from the pectorals major muscle of young donor rats were injected intramyocardially. To investigate arrhythmias, the heart's electrical activity during ischemia and the first 30 min of reperfusion were recorded by electrocardiogram. After 24 hr of reperfusion, cardiac histopathological changes, creatine kinase-MB, nitric oxide metabolites (NOx), oxidative stress markers (malondialdehyde, total anti-oxidant, superoxide dismutase, and glutathione peroxidase), and the expression of genes regulating mitochondrial fission/fusion were measured.</p><p><strong>Results: </strong>Pretreatment with CoQ₁₀ in combination with mitochondrial transplantation reduced ventricular arrhythmias, cardiac histopathological changes, and creatine kinase-MB levels. Simultaneously, this combined therapeutic approach increased myocardial NOx levels, fostering an improved oxidative balance. It also triggered the down-regulation of mitochondrial fission genes, coupled with the up-regulation of mitochondrial fusion genes.</p><p><strong>Conclusion: </strong>The combination of CoQ₁₀ and mitochondrial transplantation demonstrated a notable anti-arrhythmic effect by elevating NOx levels, reducing oxidative stress, and improving mitochondrial fission/fusion in aged rats with myocardial IRI.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"38-48"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058985","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":"Lysyl oxidase-like 2 promotes the survival, migration, and ferroptosis of endometrial cancer cells by activating the phosphoinositide 3-kinase/protein kinase B pathway.","authors":"Jiashi Gu, Huanmei Sun, Juan Shao, Hu Zhang, Zhanpeng Zhu, Dongqin Ma, Yingchun Duan","doi":"10.22038/ijbms.2024.79933.17317","DOIUrl":"10.22038/ijbms.2024.79933.17317","url":null,"abstract":"<p><strong>Objectives: </strong>LOXL2, known as Lysyl oxidase-like 2, is classified as a lysyl oxidase (LOX) family member. However, its role and mechanism in endometrial cancer (EC) are unknown. Therefore, we aimed to investigate the potential role and mechanism of LOXL2 in EC.</p><p><strong>Materials and methods: </strong>The levels of LOXL2 expression in EC tissues and normal adjacent tissues were evaluated by immunohistochemically (IHC) labeling. Following the dye application, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell methodologies were executed to evaluate the effects of LOXL2 inhibition and up-regulation on the growth, programmed cell death, migration, and susceptibility to iron-dependent cell death of EC. Moreover, protein analysis through Western blotting and gene expression analysis using Real-time quantitative PCR (RT-qPCR) was employed to measure the levels of pertinent biomarkers.</p><p><strong>Results: </strong>LOXL2 is highly expressed in both EC tissues and serum in vivo. Silencing LOXL2 reduced EC cell proliferation and migration while increasing apoptosis <i>in vitro</i>. LOXL2 silencing increased the ferroptosis-related proteins Solute Carrier Family 7 Member 11 (SLC7A11) and Ferritin Heavy Chain 1 (FTH1) while decreasing Glutathione Peroxidase 4 (GPX4) (both, <i>P<</i>0.001). Additionally, LOXL2 silencing reduced the p-PI3K and p-Akt protein expression, while LOXL2 overexpression (OE-LOXL2) elevated the p-PI3K and p-Akt protein expression (both, <i>P<</i>0.001). Additionally, LOXL2 silencing increases SLC7A11 and FTH1 while decreasing GPX4 (both <i>P<</i>0.001). LOXL2 overexpression has the opposite effect. However, the LY294002 inhibitor restores SLC7A11 and FTH1 expression while decreasing GPX4 (<i>P<</i>0.001).</p><p><strong>Conclusion: </strong>Our research demonstrated that LOXL2 might protect EC via phosphorylation by activating the PI3K/AKT pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"72-79"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059073","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":"The mTOR pathway is involved in the process of platelet-rich plasma improving intervertebral disc degeneration.","authors":"Jing Luan, Qi Wang, Wei Zheng, Yongjin He","doi":"10.22038/ijbms.2024.79218.17163","DOIUrl":"10.22038/ijbms.2024.79218.17163","url":null,"abstract":"<p><strong>Objectives: </strong>Platelet-rich plasma (PRP) contains multiple growth hormones that may stimulate tissue repair. We aimed to assess PRP's efficacy and explore possible mechanisms using the intervertebral disc degeneration (IDD) model.</p><p><strong>Materials and methods: </strong>A total of 48 male Sprague-Dawley (SD) rats were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=16, respectively). IL-1β (10 ng/ml) was used to establish a humanized IDD model in human lumbar nucleus pulposus (NP) tissues from 36 patients with degenerative disc disease. These NP cells were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=12, respectively). RT-PCR and western blot were used to detect the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, Bcl-2, cleaved-Caspase 3, Bax and Akt/mTOR/p70S6K signaling pathway. A related assay kit was used to detect MDA, SOD, and GSH.</p><p><strong>Results: </strong>PRP affected the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, MDA, SOD, GSH, Bcl-2, cleaved-Caspase 3, and Bax in IDD rats. Compared with the IDD+PBS group, the expression of <i>p-mTOR, p-p70/S6K</i>, and <i>p-Akt</i> was much lower in the rat IDD+PRP group (<i>P<</i>0.05). Similarly, with PRP treatment in the humanized IDD model, the expression of <i>p-mTOR, p-p70/S6K</i>, and <i>p-Akt</i> was also inhibited.</p><p><strong>Conclusion: </strong>PRP may be a potential therapy for IDD via the mTOR signaling pathway in regulating and affecting extracellular matrix degradation, inflammatory factors, oxidative stress, and apoptosis.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"393-400"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189148","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":"Cardiotoxicity caused by acrylamide in rats can be alleviated as a result of suppression of oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis by morin treatment.","authors":"Fatma Cakmak, Sefa Kucukler, Cihan Gur, Mustafa Ileriturk, Murat Gul, Behcet Varisli","doi":"10.22038/ijbms.2024.81490.17634","DOIUrl":"10.22038/ijbms.2024.81490.17634","url":null,"abstract":"<p><strong>Objectives: </strong>The present study investigated whether morin has a protective effect against ACR-induced cardiac toxicity.</p><p><strong>Materials and methods: </strong>In this study, oxidative stress, inflammation, endoplasmic reticulum stress (ERS), and apoptosis markers in heart tissues were analyzed by different methods after ACR (38.27 mg/kg) and morin (50 or 100 mg/kg) oral administration for ten days to Sprague Dawley rats.</p><p><strong>Results: </strong>The data obtained showed that ACR induced lipid peroxidation by decreasing superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities, glutathione (GSH) levels and nuclear factor erythroid 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase quinone 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) gene expressions. On the other hand, these markers approached the control group levels after morin treatment. Moreover, morin suppressed ACR-induced inflammatory genes. Morin down-regulated the related genes by reducing the ERS, exacerbated after ACR administration. In addition, it was observed that B-cell lymphoma-2 (Bcl-2) associated X protein (Bax), caspase-3, and apoptotic peptidase activating factor 1 (apaf-1) expressions, elevated by ACR in the heart tissue, were suppressed after morin administration. Moreover, Bcl-2 expression was triggered by morin treatment. Thus, morin suppressed ACR-induced apoptosis.</p><p><strong>Conclusion: </strong>Taken together, morin may protect against ACR-induced cardiac injury by suppressing oxidative stress, inflammation, ERS, and apoptosis.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"376-384"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189297","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}