Molecular Biology Reports最新文献

{"title":"FGFR3 gene mutations screening in non-muscle invasive bladder cancer (NMIBC) in the Tunisian population.","authors":"Bilel Saidani, Nouha Setti Boubaker, Marouen Chakroun, Haroun Ayed, Meriem Ksontini, Zeineb Naimi, Khedija Meddeb, Ahmed Saadi, Soumaya Rammeh, Mohamed Riadh Ben Slama","doi":"10.1007/s11033-025-10441-2","DOIUrl":"https://doi.org/10.1007/s11033-025-10441-2","url":null,"abstract":"<p><strong>Background: </strong>Mutations occurring in the Fibroblast Growth Factor Receptor (FGFR3) gene are thought to be associated with the incidence and prognosis of non-muscle invasive bladder tumors (NMIBC). Yet, their prognostic significance in the Tunisian population remains unclear. Herein, we aim to investigate their prognostic impact in NMIBC in terms of recurrence, progression, and survival.</p><p><strong>Methods and results: </strong>It is a monocentric retrospective study including 42 NMIBC patients. DNA was isolated from formalin-fixed paraffin-embedded tissue samples. Polymerase Chain Reaction (PCR) followed by Sanger sequencing were performed for a targeted mutations' screening of the hot-spot regions of the FGFR3 gene (exons 7 and 15). Overall survival (OS) and disease-specific survival (DSS) were estimated by the Kaplan-Meier method and the corresponding curves were compared using log-rank test. Sequencing analysis revealed 15 different mutations in FGFR3 gene across 26 different tumors (68%). Among these, 9 are already reported mutations (S249C, P250R, P250S, H251Q, S249S, S249Y, S249A, T264T, Thr651) and, interestingly, 6 are new variants (P250A, H251L, A257S, P253P, I254V, R618S). FGFR3-mutated NMIBC and wild-type FGFR3 tumors were comparable in terms of clinical and endoscopic presentation. The presence of FGFR3 mutations was not statistically correlated to a decrease in OS and DSS. The main factors correlated with their presence were the solid appearance of the tumor (p = 0.04), the presence of tumor calcifications (p = 0.04), and tumor stage (p = 0.04).</p><p><strong>Conclusion: </strong>FGFR3 mutations were common in our series. These variations seem to be a favorable prognostic factor for NMIBC in our population.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"338"},"PeriodicalIF":2.6,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular data reveal diversity of Tylodelphys spp. (Trematoda: Diplostomidae) in India: with evidence of new lineages, morphology and statistical analysis.","authors":"Komal Singh, Amit Singh Nayal, Haren Ram Chiary, Ashu Chaudhary, Sourabh Kumar, Bindu Sharma, Bhupendra Singh, Hridaya Shanker Singh, Anshu Chaudhary","doi":"10.1007/s11033-025-10456-9","DOIUrl":"https://doi.org/10.1007/s11033-025-10456-9","url":null,"abstract":"<p><strong>Background: </strong>Diplostomidae is a family of widespread digenean parasites distributed globally. The diplostomid genus Tylodelphys is frequently distributed worldwide and most published data originated from larval stages. Morphology-based identification of these parasites is typical and hard to use to identify at the species level, therefore, molecular data is needed. We cannot name these two species of Tylodelphys metacercariae yet because the adults are unknown. ITS1-5.8S-ITS2 and COX1 sequences were used for phylogenetic inference to establish the position of Tylodelphys sp. IND_ACBR1 and Tylodelphys sp. IND_ACVH1 spp. within the Diplostomoidea and to study their interrelationships with other closely related congeners.</p><p><strong>Methods and results: </strong>Tylodelphys metacercariae, infecting Ailia coila in India were collected to identify the species based on the morphology, molecular and statistical analysis. For morphology, live and stained fixed specimens were used. For molecular analysis, we have generated ITS cluster sequences (ITS1-5.8S-ITS2) of nuclear ribosomal RNA and mitochondrial cytochrome c oxidase subunit 1 (COX1) genes of Tylodelphys metacercariae. Principal component analysis (PCA) was run using R- software. Our results demonstrate that two diplostomids from India, i.e., Tylodelphys sp. IND_ACBR1 and Tylodelphys sp. IND_ACVH1 are likely undescribed taxons that belong within Diplostomidae. The results of morphology and phylogenetic analysis of both genes confirmed the status of Tylodelphys sp. IND_ACBR1 and Tylodelphys sp. IND_ACVH1 as separate species from previously published Tylodelphys species from India. The results of the statistical analysis of Tylodelphys spp. supported two distinct species status.</p><p><strong>Conclusions: </strong>The novel DNA data from this study make available chances for future appraisals of larval diplostomids, especially in India. The present study also improves our understanding of the diversity of diplostomid metacercariae larval form and offers an opportunity to study their phylogenies.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"336"},"PeriodicalIF":2.6,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The dopamine receptor agonist rotigotine attenuated indomethacin-induced enteropathy in the small intestinal mucosa of mice.","authors":"Tian Su, Li Zhou, Bingyan Peng, Wei Du, Xin Liu, Ziyu Li, Yani Zhao, Xinjie Han, Changchang Liu, Zhiyong Wang","doi":"10.1007/s11033-025-10457-8","DOIUrl":"https://doi.org/10.1007/s11033-025-10457-8","url":null,"abstract":"<p><strong>Background: </strong>Nonsteroidal anti-inflammatory drugs induced enteropathy is characterized by disruption of the epithelial barrier and immune homeostasis, resulting in symptoms such as congestion, ulcers and inflammation. Research has suggested that dopamine (DA) exerts a protective effect on the gastroduodenal and colonic mucosa. The present study aimed to explore the effect of DA on NSAID-induced injury to the small intestinal mucosa.</p><p><strong>Methods: </strong>A mouse model of enteropathy induced by indomethacin (Indo, which is a commonly used NSAID) was established by gavage. The DA agonist rotigotine (Roti) was administered alone or in combination with the DA receptor 2 (DRD2) antagonist domperidone (Domp) to model mice to determine the effect of Roti and the key role of DRD2 in this effect. Bilateral vagotomy was performed to determine whether the effect of Roti was mediated by the brain‒gut axis.</p><p><strong>Results: </strong>Roti administration attenuated small intestinal injury in Indo-induced model mice. However, Domp administration alone exacerbated this injury. Moreover, Roti mitigated small intestinal injury by increasing Occludin and zonula occludens-1 (ZO-1) expression and decreasing TNF-α and cyclooxygenase 2 (COX-2) expression. However, the effects of Roti were abrogated by Domp. In contrast to Domp, vagotomy before Indo administration did not alter the enteroprotective effects of Roti.</p><p><strong>Conclusion: </strong>The DA receptor agonist Roti attenuated Indo-induced enteropathy via peripheral DRD2 and could be a potential drug for treating NSAID-mediated enteropathy.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"335"},"PeriodicalIF":2.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143701064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Epithelial-to-mesenchymal transition based diagnostic and prognostic signature markers in non-muscle invasive and muscle invasive bladder cancer patients.","authors":"R Singh, U P Singh, V Agrawal, M Garg","doi":"10.1007/s11033-025-10450-1","DOIUrl":"https://doi.org/10.1007/s11033-025-10450-1","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"334"},"PeriodicalIF":2.6,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic diversity and evolution pattern of Plasmodium falciparum multidrug resistance 1 gene (Pfmdr1) in Indian and global populations.","authors":"Jahnvi Jakhan, Joseph Hawadak, Geetika Narang, Suman Tamang, Soumyananda Chakraborti, Vineeta Singh","doi":"10.1007/s11033-025-10424-3","DOIUrl":"https://doi.org/10.1007/s11033-025-10424-3","url":null,"abstract":"<p><strong>Background: </strong>Among the crucial molecular markers contributing to multidrug resistance, the Plasmodium falciparum multidrug resistance-1 gene (Pfmdr1) remains understudied as compared to other drug-resistant genes in terms of its genetic diversity and evolution pattern. This study presents a comprehensive analysis of Pfmdr1 gene's genetic diversity aiming to discern its dynamics, distribution and evolutionary trends especially in Indian and global populations.</p><p><strong>Methods and results: </strong>The Pfmdr1 gene was amplified and sequenced from 256 Plasmodium falciparum mono-infected samples collected from 14 Indian states during the years 1993-2023. Analysis revealed six non-synonymous (N86Y, N86F, S137C, D144F, F157L and Y184F) and one synonymous mutation (G182G) in N-terminal fragment. Among these, N86F, S137C, D144F and F157L were novel findings. The most prevalent mutations were N86Y (18.91%), Y184F (64.71%) and G182G (GGT > GGG) (59.24%; exclusive to India), with Y184F showing increasing trend when compared to N86Y over time. The mutation GGT > GGG is experiencing a hitchhiking by Y184F mutation which is likely undergoing a selective sweep. High haplotype and nucleotide diversity were observed in most Indian states, particularly in Odisha and Delhi. However, a decrease in diversity was noted in samples from 2020 onwards throughout India. Globally Pfmdr1 showed tendency of negative selection, except for populations from Liberia, Nigeria, Sudan and Central African Republic. Notably, samples from Sudan depicted a distinct haplotype and population structure compared to other countries.</p><p><strong>Conclusions: </strong>These findings contribute significantly to our understanding of the genetic structure and evolutionary trends of Pfmdr1, which can help to strengthen the current malaria control policies for emergence of drug resistance.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"332"},"PeriodicalIF":2.6,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p53-deficient cancer cells hyperactivate DNA double-strand break repair pathways to overcome chemotherapeutic damage and augment survival.","authors":"Rebecca Dsouza, Meghna Jain, Ekta Khattar","doi":"10.1007/s11033-025-10434-1","DOIUrl":"https://doi.org/10.1007/s11033-025-10434-1","url":null,"abstract":"<p><strong>Background: </strong>p53 deficiency in cancer is associated with chemoresistance and cancer progression. However, the precise role of p53 in regulating DDR in the context of chemoresistance is still unclear.</p><p><strong>Methods and results: </strong>In the present study, we investigated the regulatory role of p53 on the cellular recovery potential upon transient DNA damage. p53 deficiency promotes cell survival following transient DNA damage induction. During recovery, p53 deficient cells display temporary S/G2/M arrest, returning to normal cell cycle profile, while p53 proficient cells remain permanently arrested in the S-phase. Additionally, colony formation assay revealed 50% clonogenicity in p53-proficient cells, while p53-deficient cells showed 90% clonogenicity. Chemoresistance also correlated with accelerated DNA repair in p53-deficient cells. Since doxorubicin induces DNA double-strand breaks, whose repair is driven by two major pathways: homology-directed repair and nonhomologous end joining, we measured their activity during the recovery period. During the early recovery period, both pathways were activated irrespective of p53 expression status. However, during the late recovery time point, NHEJ and HDR activities returned to basal in p53-deficient cells, while their activity was significantly reduced in p53-proficient cells. NHEJ inhibitor Ku57788 could overcome the chemoresistance in p53-deficient cells.</p><p><strong>Conclusion: </strong>Thus, our findings suggest that sustained DDR promotes chemoresistance and enhanced survival in p53-deficient cancer cells.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"333"},"PeriodicalIF":2.6,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the role of withanolides as key modulators in breast cancer mitigation.","authors":"Huma Hameed, Maham Afzal, Mahtab Ahmad Khan, Laiba Javaid, Maria Shahzad, Kamran Abrar","doi":"10.1007/s11033-025-10442-1","DOIUrl":"https://doi.org/10.1007/s11033-025-10442-1","url":null,"abstract":"<p><p>Addressing the elaborated landscape of therapeutics of global health concern i.e. breast cancer, this comprehensive review explores the promising effects of withanolides, bioactive compounds derived from Withania somnifera, for the treatment of breast cancer. In the breast, random mutations can accumulate over time, eventually transforming it into a tumor cell as certain receptors may be overexpressed by BC cells, which elicits downstream signaling and causes the production of genes involved in angiogenesis, survival, growth and migration, and other critical cell cycle practices. Merging insights from recent studies, our exploration delves into the molecular mechanisms that highlight withanolide's potential in the intervention of breast cancer. The study of apoptotic pathways unveils the withanolide's distinctive as well as pro-apoptotic effects, hinting at its effect as a potent modulator of the progression of breast cancer cells. Beyond its independent potential, there is a discussion on its distinctive perspective over the other therapies. Inweaving together these threads of evidence illuminates channels for future research. This review acts as a guide for researchers and clinicians negotiating the challenges of incorporating withanolides into the changing landscape for the treatment of breast cancer by balancing optimism with perceptive interpretation.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"331"},"PeriodicalIF":2.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implication of the HLA-DQA1, HLA-DQB1 and CTLA-4 alleles in the susceptibility to type 1 diabetes in Jordanian population.","authors":"Monther Hussain Radi Obaied, Nazmi Ozer, Hussein Ibrahim Faleh Alawneh, Ozlem Dalmizrak","doi":"10.1007/s11033-025-10438-x","DOIUrl":"10.1007/s11033-025-10438-x","url":null,"abstract":"<p><strong>Background: </strong>Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease caused by the selective destruction of pancreatic beta cells, leading to insulin deficiency. Both genetic and environmental factors contribute to disease susceptibility. Among genetic factors, human leukocyte antigen (HLA) class II molecules, particulary DQA1 and DQB1 haplotypes, have been associated with T1D risk. This study aimed to identify haplotypes that increase susceptibility to or provide protection against T1D in Jordanian population.</p><p><strong>Methods: </strong>A total of 200 healthy individuals and 200 T1D patients were included in the study. Genomic DNA was extracted from blood samples and HLA-DQA1, HLA-DQB1 and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) gene regions were amplified by PCR. The PCR products were then subjected to restriction enzyme digestion and analyzed through agarose gel electrophoresis to determine different haplotypes.</p><p><strong>Results: </strong>Among the analyzed haplotypes, HLA-DQA1*01:01 was found to be significantly associated with increased susceptibility to T1D. In contrast, HLA-DQA1*02:01 and HLA-DQB1*05:01 appeared to provide protective effects against T1D. No significant differences were observed for other haplotypes between the control and patient groups. Additionally, no significant difference has been observed in terms of CTLA-4 polymorphisms.</p><p><strong>Conclusion: </strong>These findings suggest that HLA-DQA1*01:01 may serve as a genetic marker for T1D susceptibility, while HLA-DQA1*02:01 and HLA-DQB1*05:01 may confer protectionin the Jordanian population. Identifying these genetic risk factors could contribute to early disease prevention strategies and advanced research into additional genetic markers associated with T1D.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"330"},"PeriodicalIF":2.6,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of HLA ligands in dengue patients by multiplex PCR-SSP method.","authors":"Suwit Chaisri, Mayurachat Kaewmanee, Wisitsak Phoksawat, Chanvit Leelayuwat","doi":"10.1007/s11033-025-10420-7","DOIUrl":"https://doi.org/10.1007/s11033-025-10420-7","url":null,"abstract":"<p><strong>Background: </strong>High-throughput DNA sequencing technologies have revolutionized genetic studies of populations and diseases. These methods provide deeper insights into gene structure and variation, offering more comprehensive immunogenetic data with stronger relevance to protein function and biological impact. However, the widespread adoption of high-resolution sequencing is hindered by factors such as cost and limited accessibility. Furthermore, successful implementation requires high-quality and sufficient quantities of genomic DNA.</p><p><strong>Methods and results: </strong>This study addresses the challenges of limited DNA yields, a common issue in clinical samples, by employing whole-genome amplification (WGA) with isothermal multiple displacement amplification (IMDA). We investigated HLA ligands in 253 dengue samples with low DNA quantity. A multiplex PCR-SSP method was developed to determine HLA ligands in population, including HLA-C1, HLA-C2, HLA-A (Bw4), HLA-Bw4 (I80), HLA-Bw4 (T80), and HLA-A*11. The study successfully demonstrates the applicability of a multiplex PCR-SSP method for HLA genotyping in a large cohort of dengue patients. Our findings highlight the high prevalence of HLA-C1 (92.1%) and HLA-A*11:03 (78.3%) in dengue patients, providing valuable data for further investigations into the role of HLA polymorphisms in diseases.</p><p><strong>Conclusions: </strong>This study demonstrates the utility of our approach for investigating HLA ligands in clinical samples with limited DNA. WGA-IMDA effectively overcomes the challenge of low DNA availability, making this approach suitable for resource-constrained settings. The multiplex PCR-SSP method provides a simple and cost-effective solution for immunogenetic studies.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"328"},"PeriodicalIF":2.6,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monotropein inhibits MMP9-mediated cardiac oxidative stress, inflammation, matrix degradation and apoptosis in a mouse and cell line models of septic cardiac injury.","authors":"Wanqi Wu, Jun Wang, Guanglu Wang, Feibiao Wang, Yue Yang, Zhijun Liu, Qimei Song, Si Chen, Huizhen Chen","doi":"10.1007/s11033-025-10421-6","DOIUrl":"https://doi.org/10.1007/s11033-025-10421-6","url":null,"abstract":"<p><strong>Background: </strong>Sepsis can cause severe cardiac damage, and matrix metalloproteinase 9 (MMP9) is involved in the inflammatory response and tissue injury processes. Monotropein is a monoterpene glycoside with anti-inflammatory and antioxidant effects. This study aims to investigate whether monotropein can alleviate sepsis-induced cardiac injury by affecting the activity of MMP9.</p><p><strong>Methods and results: </strong>The correlation between MMP9 and septic cardiac injury was explored using differential expression gene analysis from the GEO database and an in vitro lipopolysaccharide (LPS)-stimulated H9c2 cell model. In a cecal ligation and puncture (CLP)-induced mouse sepsis model, the effects of monotropein on myocardial cell apoptosis, inflammatory factor expression, and antioxidant enzyme levels were validated through drug administration. The results showed that MMP9 was significantly upregulated in sepsis patients. In the H9c2 cell model, LPS-induced MMP9 activity was positively correlated with cell damage. Inhibition of MMP9 alleviates LPS-induced myocardial matrix disruption and apoptosis. Monotropein exerts anti-matrix degradation and anti-apoptotic effects through MMP9 in LPS-induced H9c2 cells. Monotropein also reduced the expression of LPS-induced inflammatory factors (TNF-α, IL-1β, IL-6).In the mouse model, monotropein decreased oxidative stress damage (lower MDA levels, increased GSH, T-AOC, CAT enzyme activity), and improved cardiac injury by inhibiting myocardial cell apoptosis-related proteins (Bax, Bcl-2, and Caspase-3 activation).</p><p><strong>Conclusion: </strong>Monotropein exerts a protective effect on septic cardiac injury by inhibiting MMP9 activity, reducing inflammatory response, and enhancing antioxidant capacity, thereby ameliorating myocardial cell damage and apoptosis.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"329"},"PeriodicalIF":2.6,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}