Naunyn-Schmiedeberg's archives of pharmacology最新文献

{"title":"Review on recent advancements in understanding acetylsalicylic acid-induced gastrointestinal injury: mechanisms, medication, and dosage refinement.","authors":"Jiahui Zhou, Na Li, Xinzhong Li, Jingxue Ye, Min Wang, Guibo Sun","doi":"10.1007/s00210-024-03521-w","DOIUrl":"10.1007/s00210-024-03521-w","url":null,"abstract":"<p><p>Acetylsalicylic acid (ASA) is a clinical drug with multiple effects, including prevention of cardiovascular adverse events and anti-cancer effects. However, gastrointestinal side effects, such as gastrointestinal ulcers and bleeding, limit the use of ASA and reduce patient compliance. Various studies have investigated the mechanisms of ASA-induced gastrointestinal injury, and many medicines have been reported to be effective in preventing and treating the adverse gastrointestinal effects of ASA. New formulations of ASA have demonstrated milder gastrointestinal injury than ASA alone. In this article, we summarized the mechanisms of ASA-induced gastrointestinal injury, drugs that resist gastrointestinal side effects of ASA, and progress in research on formulation improvement of ASA to help resolve the clinical dilemma of ASA usage.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3297-3320"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the anti-NSCLC mechanism of phillyrin targeting inhibition of the HSP90-AKT pathway.","authors":"Qiong Duan, Ruochen Li, Mingxiao Wang, Zhenting Cui, Xia Zhu, Fanghong Chen, Feng Han, Jianxin Ma","doi":"10.1007/s00210-024-03481-1","DOIUrl":"10.1007/s00210-024-03481-1","url":null,"abstract":"<p><p>Phillyrin (PHN), derived from the dried fruit of Forsythia suspensa (Thunb.) Vahl, is a kind of Chinese herbal medicine with the effect of clearing heat, and has been used in China for thousands of years in treating various tumors. However, the mechanism of its main components on non-small cell lung cancer (NSCLC) remains unclear. PHN is a distinct component extracted from Forsythia suspensa with promising anti-cancer activity against various tumor types. This study sought to elucidate the promising effects of PHN on NSCLC. Based on network pharmacology results, we identified potential PHN targets and pathways for NSCLC treatment. CCK-8 assay, wound healing assay, apoptosis assay, western blot, and in vivo experiments verified the inhibitory effect of PHN on NSCLC. Network pharmacology identified 160 potential PHN targets, 955 NSCLC-related targets, and 54 common targets, along with 132 pathways and 2 core genes. Biological experiments demonstrated that PHN significantly inhibited the growth and migration of A549 and LLC cells while promoting their apoptosis. Western blot analysis revealed down-regulation of AKT, HSP90AA1, and CDC37 expression, suggesting that PHN inhibits A549 and LLC cell proliferation by down-regulating the HSP90-AKT pathway. In vivo experiments confirmed that PHN significantly inhibited NSCLC growth with low toxicity. This study, using network pharmacology and biological experiments, verified the effectiveness of PHN against NSCLC through the HSP90-AKT pathway. These findings provide a foundation for further research and analysis.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3789-3802"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galangin prevents gentamicin-induced nephrotoxicity by modulating oxidative damage, inflammation and apoptosis in rats.","authors":"Mohammad H Abukhalil, Zina Al-Alami, Hayman A A Altaie, Saleem H Aladaileh, Sarah I Othman, Osama Y Althunibat, Manal A Alfwuaires, Afaf F Almuqati, Bader Alsuwayt, Hassan A Rudayni, Ahmed A Allam, Ayman M Mahmoud","doi":"10.1007/s00210-024-03449-1","DOIUrl":"10.1007/s00210-024-03449-1","url":null,"abstract":"<p><p>The well-known antibiotic gentamicin (GEN) works well against a variety of pathogenic bacteria, nevertheless its therapeutic use might be limited by the possibility of nephrotoxicity. The naturally occurring flavonoid galangin (GAL) has several interesting anti-inflammatory and antioxidant properties. The present study evaluated the nephroprotective effect of GAL on GEN-induced renal injury. Rats received GAL for 14 days and GEN from day 8 to day 14. There was a significant increase in serum urea and creatinine along with several histopathological changes in the kidney following GEN administration. GEN-treated rats also showed increased levels of kidney MDA and NO, and decreased GSH content and activities of antioxidant enzymes. Rats received GEN also demonstrated increased NF-κB p65, iNOS, TNF-α, IL-1β and IL-6 levels in the kidney. GAL remarkably prevented tissue injury, attenuated MDA and NO levels, improved antioxidants, and decreased levels of inflammatory mediators in the kidney of GEN-treated rats. Furthermore, GEN-administrated rats exhibited increased Bax and caspase-3 with concomitant decline in Bcl-2 levels in the kidney, an effect that GAL attenuated. In conclusion, GAL prevents GEN-induced nephrotoxicity by attenuating oxidative stress, inflammation, and apoptosis and augmenting antioxidant defense, suggesting its therapeutic potential against drug nephrotoxicity.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3717-3729"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D3 mitigates myopathy and metabolic dysfunction in rats with metabolic syndrome: the potential role of dipeptidyl peptidase-4.","authors":"Nourhan O Shoier, Salah A Ghareib, Hend Kothayer, Amira Ebrahim Alsemeh, Shaimaa S El-Sayed","doi":"10.1007/s00210-024-03439-3","DOIUrl":"10.1007/s00210-024-03439-3","url":null,"abstract":"<p><p>Metabolic syndrome is associated with vitamin D3 deficiency. This work aims to examine the efficacy of vitamin D3 in inhibiting MetS-induced myopathy and to determine whether the beneficial effects of vitamin D3 are mediated by the inhibition of dipeptidyl peptidase-4 (DPP-4). An in silico study investigated the potential effectiveness of vitamin D3 on the inhibition of the DPP-4 enzyme. An in vitro assay of the DPP-4 inhibitory effect of vitamin D3 was performed. In vivo and over 12 weeks, both diet (with 3% salt) and drinking water (with 10% fructose) were utilized to induce MetS. In the seventh week, rats received either vitamin D3, vildagliptin, a combination of both, or vehicles. Serum lipids, adipokines, glycemic indices, and glucagon-like peptide-1 (GLP-1), muscular glucose transporter type-4 (GLUT-4) content, DPP-4, adenosine monophosphate kinase (AMPK) activities, and Sudan Black B-stained lipids were assessed. Muscular reactive oxygen species (ROS), caspase-3, and desmin immunostaining were used to determine myopathy. MetS-induced metabolic dysfunction was ameliorated by vitamin D3, which also reduced intramuscular glycogen and lipid accumulation. This is demonstrated by the attenuation of MetS-induced myopathy by vitamin D3, decreased oxidative stress, increased desmin immuno-expression, and caspase-3 activity. Our in silico data demonstrated that vitamin D3 is capable of inhibiting DPP-4, which is further supported by biochemical findings. Vitamin D3 increased serum GLP-1, muscular AMPK activity, and GLUT-4 content, whereas the levels of muscular ROS were decreased in MetS. Vildagliptin and its combination with vitamin D3 yielded comparable results. It is suggested that the DPP-4 inhibitory potential of vitamin D3 is responsible for the amelioration of MetS-induced metabolic changes and myopathy.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3697-3715"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Individual and combined antagonism of aryl hydrocarbon receptor (AhR) and estrogen receptors (ERs) offers distinct level of protection against Bisphenol A (BPA)-induced pancreatic islet cell toxicity in mice.","authors":"Oly Banerjee, Tiyesh Paul, Siddhartha Singh, Bithin Kumar Maji, Sandip Mukherjee","doi":"10.1007/s00210-024-03506-9","DOIUrl":"10.1007/s00210-024-03506-9","url":null,"abstract":"<p><p>Bisphenol A (BPA), a pervasive endocrine-disrupting chemical, is known to convey harmful impact on pancreatic islets through estrogen receptors (ERs). Conversely, BPA can activate aryl hydrocarbon receptor (AhR) in certain contexts and has raised concerns about potential toxicological effects. However, BPA-AhR interaction in the context of pancreatic islet toxicity is yet to be reported. We demonstrated the specific role of AhR and its interaction with ERs to mediate BPA toxicity in pancreatic islets. In vitro, isolated islet cells treated with BPA (1 nM), with or without CH22319 (10 mM) and ICI182780 (1 mM) and insulin release, glucose-stimulated insulin secretion (GSIS), cell viability, and pERK1/2 and pAkt expression were measured. In vivo, mice were treated with BPA (10 and 100 µg/kg body weight/day for 21 days) with or without intraperitonial co-treatment of CH22319 (AhR antagonist, 10mg/kg), and ICI182780 (ER antagonist, 500 µg/kg). Glucose homeostasis, insulin resistance, oxidative stress, and inflammatory markers were measured. In vitro data revealed the involvement of AhR in the BPA-mediated alteration in insulin secretion, GSIS, and pERK1/2 and pAkt expression which were counteracted by CH223191 (AhR antagonist) alone or with ICI182780 (ER antagonist). Further, CH223191 alone or with ICI182780 modulated BPA-induced oxidative stress and pro-inflammatory cytokines and alleviated islet cell dysfunction and impaired insulin secretion. In conclusion, therapeutic targeting of AhR and ER combined might be a promising target against diabetogenic action of BPA.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3939-3954"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Facile fabrication of redox nanoparticles loaded with exosomal-miRNAs and resveratrol as glycation inhibitor in alleviating the progression and development of diabetic cataract.","authors":"Xia Chen, Qian Xi, Fei Sun, Lin Zou, Yingxuan Li","doi":"10.1007/s00210-024-03535-4","DOIUrl":"10.1007/s00210-024-03535-4","url":null,"abstract":"<p><p>Diabetic cataract (DC) represents a highly prevalent ocular manifestation resulting from diabetes often culminating in vision impairment among individuals with diabetes. Regrettably, the armamentarium of pharmaceutical interventions capable of both delaying and thwarting the onset of DC remains conspicuously sparse. Based on contemporary investigations, the pathogenesis of DC is prominently influenced by oxidative harm to the crystalline lens and the nonenzymatic glycosylation of lens proteins. Consequently, we have developed self-regenerating cerium oxide nanoparticles (CeO₂ NPs), enveloped with resveratrol (RSV) and exosomal-microRNA (miRNA) to alleviate the effects of DC in an in vitro model. Moreover, the inclusion of RSV within CeO₂ NPs serves a dual purpose. It can act as an antioxidant, minimizing glycation, and induce oxidative stress by effectively neutralizing reactive oxygen species (ROS). Additionally, it serves as a glycation inhibitor effectively preventing the cross-linking. Consequently, it helps minimize the glucose level in hemoglobin and inhibits the formation of advanced glycation end products (AGEs). Likewise, the CeO₂-exosomal-miRNA when treated alone found to slightly impede the viability of human lens epithelial cells (HLEC) and induce apoptosis by suppressing the expression of α-crystalline gene (CRYAA). Particularly, miRNAs target genes associated with oxidative stress pathways, protein glycation, and the generation of AGEs, hence preventing structural damage to lens proteins. Compared with CeO₂, RSV-CeO₂, and miRNA-RSV-CeO₂, the presence of miRNA-RSV-CeO₂ led to a significant decrease in hemoglobin glycation. Remarkably, miRNA-RSV-CeO₂ NPs attenuate the formation of malondialdehyde (MDA) and conjugated dienes (CD) with a relative value of 14.63 and 11.37 nmol/mg. As per the report, this method presents a promising opportunity to implement the proposed material combination for attenuating diabetic cataracts.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4247-4263"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synthesizing network pharmacology, bioinformatics, and in vitro experimental verification to screen candidate targets of Salidroside for mitigating Alzheimer's disease.","authors":"Yawen Cai, Guiqin Huang, Menghui Ren, Yuhui Chai, Xi Huang, Tianhua Yan","doi":"10.1007/s00210-024-03555-0","DOIUrl":"10.1007/s00210-024-03555-0","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurological disorder leading to cognitive deficits. Salidroside (Sal), a primary bioactive ingredient extracted from the roots of Rhodiola rosea L., has potent neuroprotective effects in AD. However, studies on potential targets for Sal-anchored AD are limited. In this study, we combined network pharmacology, bioinformatics, and experimental validation to identify potential targets of Sal treating AD. First, we screened 10 pyroptosis-related genes (PRGs) in Sal and AD using public databases. Then, we used Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes enrichment analysis to explore the biological functions of the shared PRGs (Sal and AD). This finding exhibited that pathways linked to inflammation, like the nucleotide oligomerization domain (NOD)-like receptors signaling pathway, are important for Sal to help fight AD. The GeneMANIA functional results subsequently revealed an association between AD and the processes of inflammasome complex and inflammatory response. Additionally, nine hub genes were identified in the protein-protein interaction network of these shared PRGs. Subsequent analysis of the genes and phenotypes confirmed that these nine hub genes were directly correlated with AD. Subsequently, an in vitro AD model was created using rat adrenal pheochromocytoma cell line (PC12) cells induced by amyloid β-peptide (Aβ) 25-35 (20 µM). Sal significantly reduced the pyroptosis caused by Aβ 25-35 in PC12 cells and decreased the expression levels of IL-1β, CASP1, IL-18, PYCARD, and NLRP3. Furthermore, molecular docking and molecular dynamics simulations confirmed that Sal could stably bind to NLRP3. Druggability analysis revealed that Sal had excellent druggability. These results demonstrated that Sal could alleviate AD by targeting IL-1β, CASP1, IL-18, PYCARD, and NLRP3 to regulate the NLRP3-mediated pyroptosis signaling pathway.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4539-4558"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging gap in treatment of polycystic ovarian syndrome through drug repurposing: what we achieved and where we are?","authors":"Popat S Kumbhar, Revati Chavan, Snehal Darekar, Kaustubh Kolekar, Anvitha Sequeira, Sukriti Vishwas, Guarav Gupta, Keshav Raj Paudel, Sachin Kumar Singh, Kamal Dua, John Disouza, Vandana Patravale","doi":"10.1007/s00210-024-03578-7","DOIUrl":"10.1007/s00210-024-03578-7","url":null,"abstract":"<p><p>Polycystic ovarian syndrome (PCOS) is one of the chief causes of infertility in women of reproductive age. Several drugs belonging to the oral contraceptive class have been approved for the treatment of PCOS. Nonetheless, the capability to target only a few symptoms of PCOS and fatal side effects are key hurdles to their use. Therefore, repurposing existing drugs can be promising in managing PCOS efficiently. Drugs from different pharmacological classes like antidiabetics (metformin, rosiglitazone, pioglitazone, and semaglutide), statins (simvastatin and atorvastatin), antiandrogen drugs (finasteride and flutamide), etc. demonstrated significant potential in managing PCOS. The present review offers a comprehensive overview of all the medications examined as potential repurposed options for the efficient treatment of PCOS. The pathogenesis of PCOS, existing therapies for PCOS and their challenges, drug repurposing and its significance is also explained. The small-molecular drugs from various pharmacological classes and different phytoceuticals repurposed against PCOS are discussed along with their anti-PCOS activity mechanisms. Moreover, novel drug targets responsible for PCOS and opportunities for drug repurposing are briefed. The repurposed drugs in clinical trials for PCOS and drug repurposing challenges are discussed. Thus, drug repurposing can serve as a potential way to effectively treat PCOS, reducing the extent of infertility and improving the quality of life of women.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3213-3240"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low molecular weight heparins promote migration and invasion of trophoblast cells through regulating the PI3K/AKT signaling pathway.","authors":"Qian Zhou, Yanan Zhao, Xiaomin Fu","doi":"10.1007/s00210-024-03577-8","DOIUrl":"10.1007/s00210-024-03577-8","url":null,"abstract":"<p><p>Pregnant women confront a high risk of mortality due to preeclampsia (PE), which also results in severe challenges for newborns. Due to their efficient properties and minimal side effects, low molecular weight heparins (LMWHs) are extensively utilized by optimizing their molecular size. Nevertheless, there have been no reports regarding the alleviating effect of LMWHs on PE and the molecular mechanism underlying it. To examine the therapeutic impact of LMWHs on PE, we initially created a PE rat model and assessed the advantages of LMWHs on PE through Western blot, immunofluorescence, TUNEL, 24-h proteinuria determination, and other techniques. Furthermore, we examined the in vitro molecular mechanism of LMWHs therapy on PE using CCK-8, Transwell, Flow cytometry, Wound healing assay, and other techniques. LMWHs, when used in vivo, reduced the rise in blood pressure and 24-h proteinuria in rat models of PE. Additionally, they prevented trophoblast cell apoptosis in these rat models. In vitro, LMWHs demonstrated a significant ability to enhance the migration and invasion of HTR-8 and JEG-3 cells. Mechanistically, LMWHs mitigate the development of PE by activating the PI3K/AKT signaling pathway. According to our findings, the activation of the PI3K/AKT signaling pathway by LMWHs appears to provide relief for PE. Therefore, we have compelling evidence supporting the use of LMWHs as an efficient treatment for PE.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"4645-4656"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin and retinal cell damage: molecular and biological functions.","authors":"Jingwen Sun, Yan Liu, Zhangming Chen","doi":"10.1007/s00210-024-03575-w","DOIUrl":"10.1007/s00210-024-03575-w","url":null,"abstract":"<p><p>The indoleamine hormone, melatonin, is produced in the pineal gland and has an essential role in many physiological functions. The pineal gland is considered to be the most important organ for producing melatonin. Nevertheless, it is important to point out that the eye is also capable of producing melatonin, and has its own circadian rhythm in producing this hormone. Melatonin is mainly produced by a subpopulation of photoreceptors in a diurnal rhythm. Numerous in vitro and in vivo studies have shown the beneficial effects of melatonin in eye-related disorders. These diseases primarily affect retinal cells, highlighting the therapeutic potential of melatonin, especially in the retina. Melatonin's ability to regulate oxidative stress response pathways and modulate the expression of antioxidant genes makes it a promising candidate for mitigating retinal cell damage. Moreover, melatonin can modulate inflammatory pathways such as NF-кB and further reduce retinal damage, as well as affecting programmed cell death such as apoptosis and autophagy in retinal cells. Therefore, the goal of this review is to explore the ways in which melatonin protects retinal cells from damage and ischemia. We discuss the mechanisms involved in order to gain valuable understanding of the possible therapeutic applications of melatonin in protection of retinal cells and treatment of retinal disorders.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":"3199-3212"},"PeriodicalIF":3.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}