Iranian Journal of Basic Medical Sciences最新文献

{"title":"Nanomolecular silencing of TSC22D4 mRNA via a DNAsome-siRNA for enhancing insulin sensitization in hepatocytes.","authors":"Ameneh Mohammadi, Pedram Ebrahimnejad, Said Abediankenari, Zahra Kashi, Pooria Gill","doi":"10.22038/ijbms.2024.81998.17744","DOIUrl":"10.22038/ijbms.2024.81998.17744","url":null,"abstract":"<p><strong>Objectives: </strong>Insulin resistance (IR) is a critical component of metabolic syndrome, primarily linked to obesity. It contributes to impaired glucose metabolism, beta-cell dysfunction, and the onset of type 2 diabetes. This study aimed to develop a DNAsome nanocarrier designed for the targeted delivery of small interfering RNA (siRNA) to inhibit mRNA of Transforming growth factor beta-like Stimulated Clone 22 D4 (TSC22D4), thereby enhancing insulin sensitivity in hepatocytes.</p><p><strong>Materials and methods: </strong>The DNAsome was constructed using Y-DNA building blocks derived from three distinct DNA oligonucleotides. Its structural characteristics were analyzed through atomic force microscopy (AFM). The functional efficacy of the DNAsome in delivering siRNA was evaluated by measuring its cellular uptake and ability to down-regulate TSC22D4 expression in HepG2 cells via real-time PCR. Additionally, the cytotoxicity and safety of both the DNAsome and the DNAsome-siRNA complexes were assessed using the MTT assay on HepG2 cells.</p><p><strong>Results: </strong>Findings indicated successful fabrication of the DNAsome nanocarriers, although aggregation was observed at higher concentrations, yielding nanoparticle sizes between 116 and 740 nm. Real-time PCR results confirmed effective siRNA targeting, significant cellular uptake of the nanocomplexes, and successful silencing of TSC22D4 expression.</p><p><strong>Conclusion: </strong>This study suggests that DNAsome-based siRNA delivery systems hold promise for improving insulin sensitivity and addressing IR associated with obesity and metabolic syndrome.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"385-392"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189059","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":"Assessing the efficacy of herbal supplements for managing obesity: A comprehensive review of global clinical trials.","authors":"Mahboobeh Ghasemzadeh Rahbardar, Gordon A Ferns, Majid Ghayour Mobarhan","doi":"10.22038/ijbms.2025.84150.18198","DOIUrl":"https://doi.org/10.22038/ijbms.2025.84150.18198","url":null,"abstract":"<p><p>Obesity remains a significant worldwide health concern, and further research into other strategies, including herbal weight-loss medications, is necessary. By reviewing clinical trials, this study aims to evaluate the effectiveness of herbal medicines for weight loss or obesity. A comprehensive search was conducted using multiple databases. Clinical trials evaluating the effects of herbal medicines on weight loss or obesity management were included. Relevant data, such as study design, intervention details, and outcome measures, were extracted and analyzed. The use of herbal medicines exhibited varying efficacy in promoting weight loss or managing obesity. Some herbal interventions significantly reduced body weight, body mass index (BMI), and waist circumference. Notably, these interventions led to decreases in fasting blood glucose (FBG) and homeostatic model assessment of insulin resistance (HOMA-IR), regulating insulin levels while increasing levels of catalase (CAT) and glutathione (GSH). Additionally, reductions in inflammatory markers such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-alpha (TNF-α) were observed, indicating a potential anti-inflammatory effect. Mechanisms of action included appetite regulation, fat oxidation, increased satiety, enhanced insulin sensitivity, and modulation of lipid metabolism. However, it is important to note that these herbal interventions' efficacy and safety profiles may vary among different population groups. The findings suggest that certain herbal medicines hold promise as adjunctive therapies for weight loss and obesity management. However, comprehensive and targeted research efforts are warranted to determine these herbal interventions' optimal use, dosages, and long-term effects in specific population subgroups.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"691-709"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990661","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":"Black seed oil nanoemulsion containing albendazole against protoscoleces of <i>Echinococcus granulosus</i>: An <i>in vivo</i> study on C57BL/6 mice.","authors":"Fatemeh Oroojalian, Tahereh Mohammadzadeh, Ailin Ebrahimzadeh, Peiman Alesheikh, Reza Shafiei, Amir Amani","doi":"10.22038/ijbms.2025.83014.17942","DOIUrl":"https://doi.org/10.22038/ijbms.2025.83014.17942","url":null,"abstract":"<p><strong>Objectives: </strong>Hydatid cysts are typically treated with albendazole. Nevertheless, this drug has side effects and limited bioavailability. In this study, we aimed to explore a nanoemulsion of black seed oil to enhance the therapeutic efficacy of albendazole in mice with hydatid cysts.</p><p><strong>Materials and methods: </strong>The size of the prepared nanoemulsions was characterized using a Zetasizer analyzer. Additionally, the stability of the nanoemulsions was assessed after 45 days. MTT assay was used to compare the cytotoxicity of free albendazole, nanoemulsion containing albendazole, and nanoemulsion without albendazole. Furthermore, infected mice were treated with these preparations, euthanized, and subjected to autopsy examination. Cysts obtained from mice were examined for histopathological features.</p><p><strong>Results: </strong>ALB-NE (albendazole-loaded nanoemulsion) DLS results were obtained from black seed oil. Freshly prepared ALB-NE showed (d50 = 170 nm), PDI: 0.323, ALB-NE after 45 days storage at 25 ºC were (d50 = 92.4 nm), and ALB-NE after 45 days storage at 45 ºC revealed (d50 = 118 nm). The cytotoxicity of albendazole was reduced when loaded into the nanoemulsion. Moreover, the group treated with nanoemulsion containing albendazole showed a significant decrease in size and number of cysts compared to those receiving free albendazole or nanoemulsion without the drug. Additionally, after 60 days, the nanoemulsion containing albendazole showed 100% survival, while the survival rate was 50% for free albendazole, 75% for nanoemulsion without albendazole, and 37.5% for PBS.</p><p><strong>Conclusion: </strong>The nanoemulsion containing albendazole can be a promising treatment for hydatid cysts.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"755-761"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980961","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":"EGCG attenuated spinal cord injury by inhibiting ferroptosis via activation of HMOX1 expression and suppression of HIF-1 signaling pathway.","authors":"Han Yang, Fei Ye, Liuxu Chen, Linyu Yang, Jianping Kang","doi":"10.22038/ijbms.2025.82651.17864","DOIUrl":"https://doi.org/10.22038/ijbms.2025.82651.17864","url":null,"abstract":"<p><strong>Objectives: </strong>Epigallocatechin gallate (EGCG) exhibits various biological effects, including antiviral, anti-inflammatory, cardioprotective, and lipid-regulating properties. This study aims to investigate the therapeutic effects and mechanisms of EGCG in spinal cord injury (SCI).</p><p><strong>Materials and methods: </strong>The bioinformatic databases were used to screen therapeutic target genes for drugs against SCI. Component-Target-Disease networks were constructed with Cytoscape software, and inter-target interactions were analyzed using the String database. Additionally, KEGG pathway enrichment analyses were conducted on the identified target genes. SCI was evaluated by detecting inflammation-related factors, H&E staining, and immunohistochemistry. Furthermore, ROS and JC1 staining were performed on HT22 cells subjected to various treatments. Molecular mechanisms were investigated using western blot and qRT-PCR analyses.</p><p><strong>Results: </strong>Forty-four overlapping genes were identified as potential targets, with HMOX1, GPX-4, and HIF-1A emerging as central hub genes. Key pathways associated with these targets included Ferroptosis and HIF-1 signaling. <i>In vivo</i> studies demonstrated that EGCG effectively promotes motor function recovery and reduces the expression of proteins and genes such as IL-1β, IL-6, HIF-1α, and 4HNE. <i>In vitro</i> experiments showed that EGCG decreases ROS and intracellular lipid ROS levels in HT22 cells while increasing GPX-4 and HMOX1 expression to inhibit ferroptosis and HIF-1 signaling pathways.</p><p><strong>Conclusion: </strong>Our findings reveal a significant new mechanism by which EGCG can reduce SCI through the inhibition of ferroptosis, facilitated by the activation of HMOX1 expression and the down-regulation of the HIF-1 signaling pathway. This suggests its potential as a therapeutic option for this condition.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"799-807"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012858","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":"Mechanism of action of total saponin Achyranthes in treating knee osteoarthritis explored using network pharmacology and animal experimentation.","authors":"Shiwei Zhuang, Qiang Chen, Xiao Guo, Wenhai Zhao, Ye Qiu","doi":"10.22038/ijbms.2025.83153.17974","DOIUrl":"https://doi.org/10.22038/ijbms.2025.83153.17974","url":null,"abstract":"<p><strong>Objectives: </strong>Knee osteoarthritis (KOA) is a persistent degenerative disease affecting the joints, significantly reducing the quality of life for individuals afflicted. This study explores the therapeutic effects of total saponin Achranthes (TSA) on KOA rats and its underlying mechanism.</p><p><strong>Materials and methods: </strong>Forty-eight rats were randomly assigned to six experimental groups: a blank control group, a model group, a sham-operated group, and a TSA treatment group (low, medium, and high dose), with eight rats in each group. The rats were treated continuously for four weeks. The degree of joint swelling was quantified, and the Lequesne MG score was evaluated. Network pharmacology approaches were employed to pinpoint potential TSA targets and related pathways for managing KOA. Additionally, histopathological examinations were conducted on the knee cartilage of the rats. Serum levels of TNF-α and IL-1β were assessed through the ELISA assay.</p><p><strong>Results: </strong>The network pharmacology results indicate that TSA may effectively treat KOA through the MAPK and PI3K/Akt signaling pathways. Moreover, TSA significantly decreased the serum concentrations of pro-inflammatory cytokines such as TNF-α and IL-1β, and TSA down-regulated the P38 MAPK, PI3K/Akt, and NF-κB pathways, whereas the KOA model showed up-regulation. The treatment also significantly reduced MMP-9, MMP-13, and ADAMTS-5 protein levels.</p><p><strong>Conclusion: </strong>TSA can potentially ameliorate inflammation, safeguard knee cartilage tissue, and alleviate symptoms of KOA by inhibiting the MAPK/Akt/NF-κB signaling pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 6","pages":"762-771"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12057757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005088","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":"Ellagic acid alleviates NLRP6/caspase-1/GSDMD-mediated inflammation and pyroptosis in rats post cerebral ischemia/reperfusion injury.","authors":"Ling Hu, Xiaoqiong Wei, Guofu Shen, Xiaohuan Huang","doi":"10.22038/ijbms.2024.78864.17057","DOIUrl":"10.22038/ijbms.2024.78864.17057","url":null,"abstract":"<p><strong>Objectives: </strong>Ellagic acid (EA) is a natural polyphenol with anti-cancer, anti-oxidant, anti-inflammatory, antibacterial, and other effects. However, the role of EA in cerebral ischemia/reperfusion injury (CIRI) remains unclear. This study aims to investigate the neuroprotective effects of EA in CIRI.</p><p><strong>Materials and methods: </strong>Forty male Wistar rats (260-300 g) were randomly divided into four groups with 10 rats per group: 1) Sham+Veh: Rats underwent I/R surgery, except that they were not inserted with thread plugs, and received solute treatment at the same time. 2) MCAO/R+Veh. 3) MCAO/R+EA: Rats were administered 200 mg/kg EA before undergoing MCAO. 4) MCAO/R+Nim: Rats were administered Nim before undergoing MCAO.</p><p><strong>Results: </strong>Cerebral MCAO/R damaged brain tissue, elevated neurological deficit score (<i>P<</i>0.01), cerebral infarction volume (<i>P<</i>0.01), inflammatory cell infiltration (<i>P<</i>0.01), NLRP6, ASC, caspase-1 and GSDMD mRNA level (<i>P<</i>0.01 and <i>P<</i>0.001), NLRP6, caspase-1, GSDMD-N and IL-1β protein level (<i>P<</i>0.01 and <i>P<</i>0.001), and inflammatory cytokines in brain tissue (<i>P<</i>0.01). Prophylactic administration of EA also significantly improved brain tissue damage, reduced neurological deficit score (<i>P<</i>0.01), cerebral infarction volume (<i>P<</i>0.01), inflammatory cell number (<i>P<</i>0.05), NLRP6, caspase-1, GSDMD-N mRNA and protein level (<i>P<</i>0.05 and <i>P<</i>0.01), ASC mRNA level and IL-1β protein level (<i>P<</i>0.01), and IL-1β and IL-18 level in brain tissue (<i>P<</i>0.01) compared to positive control.</p><p><strong>Conclusion: </strong>EA may serve as a potential drug for the treatment of brain I/R, which may exert an anti-inflammatory effect by inhibiting the activation of the inflammasome.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"105-112"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058959","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":"Endurance training and pyruvate dehydrogenase kinase 4 (PDK4) inhibition combination is superior to each one alone in attenuating hyperketonemia/ketoacidosis in diabetic rats.","authors":"Hamed Rezaeinasab, Abdolhamid Habibi, Ramin Rezaei, Aref Basereh, Salva Reverentia Yurista, Kayvan Khoramipour","doi":"10.22038/ijbms.2024.79864.17305","DOIUrl":"10.22038/ijbms.2024.79864.17305","url":null,"abstract":"<p><strong>Objectives: </strong>While ketone bodies are not the main heart fuel, exercise may increase their uptake. Objectives: This study aimed to investigate the effect of 6-week endurance training and Pyruvate dehydrogenase kinase 4 )PDK4( inhibition on ketone bodies metabolism in the heart of diabetic rats with emphasis on the role of Peroxisome proliferator-activated receptor-gamma coactivator PGC-1alpha (PGC-1α).</p><p><strong>Materials and methods: </strong>Sixty male Wistar rats were divided into eight groups: healthy control group (CONT), endurance training group (TRA), diabetic group (DM), DM + EX group, Dichloroacetate (DCA) group, DM + DCA group, TRA + DCA group, and DM + TRA + DCA group. Diabetes was induced using streptozotocin (STZ). The animals in training groups ran on the treadmill for six weeks (30-50 min running at 20-30 m/min). After the training period, molecular markers for mitochondrial biogenesis and ketone metabolism were assessed in the heart. Circulating ß-hydroxybutyrate (ßOHB) and Acetylacetonate (AcAc) levels were also measured.</p><p><strong>Results: </strong>Our results showed that 6-week endurance training increased the cardiac expression of PGC-1α, 3-oxoacid CoA-transferase 1 (OXCT1), and Acetyl-CoA Acetyltransferase 1 (ACAT1) and reduced beta-hydroxybutyrate dehydrogenase1 (BDH1) expression (<i>P</i>≤0.05). In addition, exercise and DCA usage significantly decreased PDK4 gene expression, ßOHB, and AcAc blood levels (<i>P</i>≤0.05). Furthermore, the combination of 6-week endurance training and DCA supplementation led to more reduction in PDFK4 gene expression, ßOHB, and AcAc blood levels.</p><p><strong>Conclusion: </strong>Six-week endurance training and DCA supplementation could safely improve ketone body metabolism in the heart, ultimately reducing hyperketonemia/ketoacidosis in diabetic rats.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 1","pages":"80-86"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059071","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":"Microsomal glutathione transferase 1 confers cisplatin resistance of non-small cell lung cancer via interaction with arachidonate lipoxygenase 5 to repress ferroptosis.","authors":"Jun Yuan, Rui Zhang, Li Liu, Yue-Song Ban, Ce Qin","doi":"10.22038/ijbms.2024.79203.17160","DOIUrl":"10.22038/ijbms.2024.79203.17160","url":null,"abstract":"<p><strong>Objectives: </strong>Cisplatin (DDP) resistance remains a primary cause of chemotherapy failure and recurrence of non-small cell lung cancer (NSCLC). Abnormal high microsomal glutathione transferase 1 (MGST1) expression has been found in DDP-resistant NSCLC cells. This study aimed to explore the function and mechanism of MGST1 in DDP resistance of NSCLC cells.</p><p><strong>Materials and methods: </strong>The expression levels of target molecules were assessed by quantitative real-time polymerase chain reaction (RT-qPCR) and western blotting. Cell proliferation was evaluated by cell counting kit-8 (CCK-8) and colony formation assays. Ferroptosis was determined by malondialdehyde (MDA), glutathione (GSH), Fe²⁺, and reactive oxygen species (ROS) levels. The interaction between proteins was confirmed by Co-immunoprecipitation (Co-IP). The effect of MGST1 on DDP resistance was evaluated using the tumor xenograft assay in vivo. Immunohistochemical staining was performed to measure Ki-67 and p-H2A.X expression in tumor tissues.</p><p><strong>Results: </strong>MGST1 expression was higher, while arachidonate lipoxygenase 5 (ALOX5) expression was lower in DDP-resistant NSCLC patients and cells. <i>MGST1</i> ablation sensitized NSCLC cells to DDP therapy through inducing ferroptosis. MGST1 protein directly interacted with ALOX5 protein to restrain ALOX5-triggered ferroptosis. Ferroptosis inhibitor or sh-ALOX5 reversed the promotive effect of MGST1 silencing on the DDP sensitivity of NSCLC cells. Finally, <i>MGST1</i> depletion sensitized NSCLC cells to DDP therapy in nude mice <i>in vivo</i>.</p><p><strong>Conclusion: </strong>MGST1 high expression contributed to DDP resistance of NSCLC cells by inhibiting ALOX5-induced ferroptosis. Our results provide a potential therapeutic target for overcoming DDP resistance in NSCLC patients.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"209-216"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028723","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":"Vanillic acid as a promising intervention for metabolic syndrome: Preclinical studies.","authors":"Mahboobeh Ghasemzadeh Rahbardar, Gordon A Ferns, Majid Ghayour Mobarhan","doi":"10.22038/ijbms.2024.81709.17680","DOIUrl":"10.22038/ijbms.2024.81709.17680","url":null,"abstract":"<p><p>Metabolic syndrome is a clustering of metabolic abnormalities and anthropometric factors that increase the risk of cardiovascular disease and type 2 diabetes mellitus. As the search for effective treatments intensifies, attention has turned towards natural substances with potential medicinal benefits. Among them, vanillic acid, a phenolic acid present in many plants, has attracted some attention due to its wide range of biological activities. This review aimed to provide an in-depth summary of the potential therapeutic use of vanillic acid in metabolic syndrome. The potential mechanisms of action of vanillic acid, including its anti-oxidant, anti-inflammatory, and hypolipidemic properties, are discussed. The effect of vanillic acid on glucose homeostasis, insulin sensitivity, and adipocyte activity is also addressed. The effect of vanillic acid on lipid metabolism, including the control of lipid synthesis, breakdown, and transport, is also reviewed. The emerging evidence for the beneficial effects of vanillic acid in animal models, <i>in vitro</i> studies, and preliminary clinical studies is also highlighted. The data suggests that vanillic acid has the potential to ameliorate metabolic syndrome. However, further preclinical and clinical research is needed to determine the specific mechanisms of action, appropriate dose, and subsequent advantages of vanillic acid. A more comprehensive understanding of the therapeutic potential of vanillic acid could pave the way for developing innovative techniques for preventing and treating metabolic syndrome and its implications.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 2","pages":"141-150"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028786","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 bacteria in cancers and their therapeutic potential: Review of current knowledge.","authors":"Wojciech Wawrety, Anna Kedziora","doi":"10.22038/ijbms.2024.77667.16798","DOIUrl":"10.22038/ijbms.2024.77667.16798","url":null,"abstract":"<p><p>Cancers are extremely dynamic diseases that can actively cause refractorines to be gained from applied therapies, which is why they are at the forefront of deaths worldwide. In this literature review, we covered the most recent and important discoveries regarding the influence of human microbiota, including tumor bacteriome, on the development and treatment of cancer. Advances in research on microbial communities have enabled us to discover the role of the human microbiome in the development and course of this disease, helping us understand neoplasms better and design new potential therapies. As we show through our findings, by immunomodulation and the secretion of certain chemical substances, the correct bacteriome of the intestinal tract, respiratory system, or skin can protect humans against cancer development and help during the treatment process. Bacteria also reside inside tumors, forming part of the tumor microenvironment (TME), where they interact with immunological and cancer cells in many complex ways. Some bacteria, such as <i>Pseudomonas aeruginosa</i> or <i>Akkermansia muciniphila</i>, can stimulate anticancer cell-mediated immune responses or even directly lead to cancer cell death. We also present the clinical possibilities of using some live, usually modified bacteria to develop bacteriotherapies. Modifying the gut microbiome to stimulate standard treatment is also important. Research on the microbiome and cancer remains a challenging topic in microbiology, having a great potential for advancements in cancer therapy in the future, and is continuously becoming a more and more popular field of research, as shown by our statistical analysis of PubMed data.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"28 3","pages":"273-282"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189086","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}