Pharmacological Research - Reports最新文献

{"title":"The role of interleukin-1 beta in inflammation and the potential of immune-targeted therapies","authors":"Syed Ali Wijdan ,&nbsp;Syed Muhammad Nasir Abbas Bokhari ,&nbsp;Jenelle Alvares ,&nbsp;Varisha Latif","doi":"10.1016/j.prerep.2025.100027","DOIUrl":"10.1016/j.prerep.2025.100027","url":null,"abstract":"<div><div>Interleukin-1 beta (IL-1β) has emerged as an important therapeutic target, due to its key role in mediating inflammation and tissue damage in different disorders. This study presents a thorough review of the conditions in which (IL-1β) is playing an important role and a summary of the new and ongoing treatments aimed at suppressing its activity. Furthermore, we explored currently available IL-1β targeted treatments, such as IL-1 inhibitors like Canakinumab and Anakinra, and also explained their work at molecular level in reducing inflammation. IL-1β is targeted in inflammatory illnesses in treatment that are beneficial, but there are drawbacks as well which includes the requirement for customized treatment plans, drug resistance, and unpleasant effects. This study also underlines the recent advancements in IL-1β targeted therapies, shedding light on novel approaches.</div></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"3 ","pages":"Article 100027"},"PeriodicalIF":0.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143152927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional analysis of quinovic acid derivatives from Sarcocephalus pobeguinii as inhibitors of hepatitis C virus NS3/4A protease","authors":"Arnaud Fondjo Kouam ,&nbsp;Aristide Mfifen Munvera ,&nbsp;Jordas Casares Tchana Tchamba ,&nbsp;Elisabeth Menkem Zeuko’o ,&nbsp;Armelle Gaelle Kwesseu Fepa ,&nbsp;Brice Fredy Nemg Simo ,&nbsp;Felicité Syntia Douanla Somene ,&nbsp;Armel Jackson Seukep ,&nbsp;Pierre Mkounga ,&nbsp;Jules Clément Nguedia Assob ,&nbsp;Frédéric Nico Njayou ,&nbsp;Paul Fewou Moundipa","doi":"10.1016/j.prerep.2024.100026","DOIUrl":"10.1016/j.prerep.2024.100026","url":null,"abstract":"<div><div>This study assessed compounds from <em>Sarcocephalus pobeguinii</em> as potential inhibitors of HCV-NS3/4 A. Ten compounds isolated from <em>S. pobeguinii</em> were initially screened for their inhibitory activity against HCV-NS3/4 A through the fluorescence resonance energy transfer assay. The 50 % inhibitory concentration (IC₅₀) and the inhibition mechanism of active compounds were determined through concentration-response and enzyme-kinetics studies, respectively. The physical interactions between the enzyme and inhibitors were analyzed by thermal shift assay and surface plasmon resonance, while molecular interactions were predicted using molecular docking. The antiviral activity of the hit compounds was tested in a cell-based assay. Three inhibitors of HCV-NS3/4 A: Quinovic acid, Quinovic acid 3-O-[α-D-quinovopyranoside], and Quinovic acid 3-O-[β-D-quinovopyranoside] with IC₅₀ in the micromolar range were successfully identified. They displayed their inhibitory activity through a non-competitive inhibition mechanism and bound to the HCV-NS3/4 A protease in a real-time manner through 1:1 binding and steady-state affinity models, inducing its instability by lowering its melting temperature. The lead compounds effectively inhibited HCV replication at non-toxic concentrations. These results contribute to the valorization of <em>S. pobeguinii</em> as a potential source of efficient inhibitors to reinforce the current therapeutic arsenal for the treatment of HCV infection.</div></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"3 ","pages":"Article 100026"},"PeriodicalIF":0.0,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143151992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Canagliflozin attenuates haloperidol-induced motor and spatial working memory deficits in mice: Evidence of its role in the treatment of Parkinson’s disease","authors":"Emmanuel Semasa Irokosu ,&nbsp;Farouk Adedeji Oladoja ,&nbsp;Sunday O. Olayemi ,&nbsp;Ismail O. Ishola","doi":"10.1016/j.prerep.2024.100025","DOIUrl":"10.1016/j.prerep.2024.100025","url":null,"abstract":"<div><div>Canagliflozin (CANA), a sodium-glucose cotransporter-2 (SGLT-2) inhibitor, has been widely reported for its neuroprotective activity evidenced by its antioxidant and anti-inflammatory properties in brain tissue injury. Thus, it is a promising therapeutic candidate in the treatment of neurodegenerative diseases. This study examined the protective effect of CANA on haloperidol-induced Parkinsonism in mice. Forty-two male mice were divided randomly into seven groups: group 1 - normal control; vehicle (10 mL/kg, <em>p.o</em>.), group 2 - vehicle (pathological control; 10 mL/kg, per oral), groups 3–5, received CANA (25, 50, and 100 mg/kg, <em>p.o</em>., respectively), and the sixth and seventh groups received trihexyphenidyl (THP, 1 mg/kg, <em>p.o.,</em> standard drug), and CANA 100 mg/kg respectively, for 21 consecutive days. Animals in groups 2–6 were given haloperidol (1 mg/kg, <em>i.p</em>.) daily, one hour after pretreatment for 21 days. Spontaneous motor functions assessed with bar and rotarod test as well as working memory by Y-maze test. Thereafter, blood and discrete brain regions were collected for biochemical assays. CANA (25, 50, and 100 mg/kg) demonstrated significant reduction in cataleptic scores in both acute (22, 58, and 76 %, respectively) and chronic (46, 61, and 69 %, respectively) in bar tests at 120 minutes. CANA improved motor coordination through prolongation of latency to fall in the rotarod test. Similarly, haloperidol-induced working memory impairment was reversed by CANA evidenced in significant increase percent alternation behaviour and counteracted dopamine depletion by 57 and 68 % at 50 and 100 mg/kg, respectively. Furthermore, CANA significantly attenuated haloperidol-induced oxidative stress and TNF-α induction. It is of note that CANA did not induce hypoglycaemia in any of the treatment group. Findings from our study demonstrated the ability of canagliflozin to control muscle spasticity/weakness and working memory impairment in Parkinsonism through attenuation of oxidative stress and neuroinflammation.</div></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"3 ","pages":"Article 100025"},"PeriodicalIF":0.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143152926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pretreatment with acetylsalicylic acid alleviates UVB irradiation-induced skin pathology in hairless mice and BOC-2 (an ALX/FPR2 receptor antagonist) reduces its activity","authors":"Renata M. Martinez ,&nbsp;Priscila Saito ,&nbsp;Ingrid C. Pinto ,&nbsp;Camilla C.A. Rodrigues ,&nbsp;Victor Fattori ,&nbsp;Cristina P.B. Melo ,&nbsp;Allan J.C. Bussmann ,&nbsp;Larissa Staurengo-Ferrari ,&nbsp;Tiago H. Zaninelli ,&nbsp;Telma Saraiva-Santos ,&nbsp;Michel F. Otuki ,&nbsp;Daniela A. Cabrini ,&nbsp;Marcela M. Baracat ,&nbsp;Sandra R. Georgetti ,&nbsp;Waldiceu A. Verri Jr. ,&nbsp;Rubia Casagrande","doi":"10.1016/j.prerep.2024.100024","DOIUrl":"10.1016/j.prerep.2024.100024","url":null,"abstract":"<div><div>This work aims to investigate if the biological activity of acetylsalicylic acid (ASA) against UVB irradiation-induced skin inflammatory and oxidative injury in hairless mice would be amenable by treatment with BOC-2, an antagonist of the formyl peptide receptor 2 receptor (ALX/FPR2). Mice were treated with BOC-2 and after 30 minutes, they received ASA or Aspirin-Triggered 15-epi-lipoxin A₄ (AT-LXA_4, an agonist of ALX/FPR2), and after 1 hour, they were exposed to UVB irradiation (dose of 4.14 J/cm²). UVB stimulation induced neutrophil and mast cell recruitment, edema, matrix metalloproteinase-9 (MMP-9) activity, collagen degradation, sunburn cell formation, and cytokine production (TNF-α, IL-1β and IL-6). All these parameters were inhibited by ASA or AT-LXA₄. In addition, ASA and AT-LXA₄ enhanced anti-inflammatory cytokines (IL-10 and TGF-β), and attenuated UVB-induced oxidative damage returning the oxidative status to baseline levels in parameters such as ferric reducing ability, free radical scavenging, reduced glutathione levels, catalase activity, superoxide anion production, Nrf2, Nqo1, and gp91^phox mRNA expression. These therapeutic effects of ASA and AT-LXA₄ were reversed by BOC-2. Our results demonstrate that ALX/FPR2 receptor plays an important role in ASA activity against UVB-induced skin pathologies.</div></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"3 ","pages":"Article 100024"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143152928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bilirubin, a potent and persistent inhibitor of genetic damage induced by gamma rays in D. melanogaster","authors":"Elizabeth Jiménez ,&nbsp;Emilio Pimentel ,&nbsp;Martha P. Cruces ,&nbsp;Viviana Valadez-Graham ,&nbsp;Zazil Velázquez","doi":"10.1016/j.prerep.2024.100022","DOIUrl":"10.1016/j.prerep.2024.100022","url":null,"abstract":"<div><div>The antimutagenic and radioprotective action as well as the persistence of the effects of chlorophyllin, a tetrapyrrole with copper-chelate ring, was demonstrated in our laboratory, using the <em>in vivo</em> system <em>Drosophila melanogaster</em>. The aim of this investigation was to evaluate the inhibitory capacity of bilirubin (BRB) on gamma radiation-induced oxidative genetic damage. For this purpose, the SMART assay on the wing of <em>D. melanogaster</em> was used. Second instar larvae were pretreated with BRB for 24 hours and then groups of them were exposed to gamma ray at 0, 24, 48 or 72 hours after pretreatment. For the antioxidant action, Canton-S strain larvae were pretreated during 2 h with BRB, and after that, they were exposed to gamma rays to measure the activity of the SOD, CAT and GSH-Px enzymes and overexpression of genes <em>Sod</em> and <em>Cat</em>. The results indicated that the group treated with BRB+Gamma rays sharply reduced (56 %) the genetic damage compared to the groups exposed only to gamma rays. Furthermore, this effect was persistent up to 72 h after pretreatment. Bilirubin did not modify CAT nor GSH-Px enzymes activity, neither the transcription of <em>Sod1</em> gene at any time tested, however, the <em>Cat</em> gene only overexpressed 24 h after BRB and BRB+10 Gy treatment. These findings suggest that these porphyrins act as antioxidants probably by itself, which positions BRB as a possible radioprotector.</div></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100022"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142705857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discovery of novel peptide deformylase inhibitors: Ensemble complex-based pharmacophore modeling, docking and binding affinity studies","authors":"Vijaya Bhaskar Baki ,&nbsp;Siva Rajesh Sivarathri ,&nbsp;Munichandra Babu Tirumalasetty ,&nbsp;M.V. Jyothi Kumar ,&nbsp;Rammohan Aluru","doi":"10.1016/j.prerep.2024.100011","DOIUrl":"10.1016/j.prerep.2024.100011","url":null,"abstract":"<div><p><em>Pseudomonas aeruginosa</em> infections are quickly increasing in association with a variety of illnesses, necessitating the development of novel medications. This study employed an <em>in silico</em> technique to find PDF inhibitors against <em>P. aeruginosa</em> Peptide deformylase (PaPDF). PaPDF's structure is comparable to that of other PDFs; however, binding site studies found that PaPDF has a smaller pocket than <em>Staphylococcus aureus</em>, covering the S1 and S2 sub pockets, and maintains a conserved hydrophobic nature. The Zn metal binding site of modified PaPDFs was examined using molecular dynamics, and the results revealed that Cys92Ala differed from His134Ala and His138Ala, respectively. Complex-based pharmacophore investigation revealed three significant pharmacophoric characteristics within the pocket: two hydrophobic and one H-bond acceptor. This allows us to perform virtual screening using the ChemBride database to uncover a variety of potential hits with specific inhibitory characteristics. Several restrictions, including docking and molecular mechanics/general born-volume integral implicit solvent (MM/GBVI), were applied, and the top-ranked ligands were tested for inhibitory characteristics against key residues in the active site. Furthermore, the bioavailability and toxicity prediction identified seven potential leads and suggested future research into the design and synthesis of a unique class of PaPDF inhibitors.</p></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100011"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950200424000119/pdfft?md5=31489a4403fc10c617aba7dc8b969fb5&pid=1-s2.0-S2950200424000119-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141390792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The synthetic peptide, PnPP-15, derived from the PnTx2-6 toxin of the spider Phoneutria nigriventer, induces peripheral antinociception involving neprilysin, opioid, and cannabinoid systems","authors":"Renata Cristina Mendes Ferreira ,&nbsp;Edleusa Marques Lima-Batista ,&nbsp;Ana Cristina Nogueira Freitas ,&nbsp;Xavier Maia Mariano ,&nbsp;Marcelo Ferreira Marcondes Machado ,&nbsp;Dongchen Na ,&nbsp;Adriana Karaoglanovic Carmona ,&nbsp;Steve Peigneur ,&nbsp;William Gustavo Lima ,&nbsp;Brener Cunha Carvalho ,&nbsp;Carlos Alberto Tagliati ,&nbsp;Jan Tytgat ,&nbsp;Igor Dimitri Gama Duarte ,&nbsp;Maria Elena de Lima","doi":"10.1016/j.prerep.2024.100012","DOIUrl":"https://doi.org/10.1016/j.prerep.2024.100012","url":null,"abstract":"<div><h3>Background</h3><p>The PnTx2–6 toxin is isolated from the Phoneutria nigriventer spider venom. The synthetic peptide PnPP-19 is derived from this toxin and induces antinociception. When topically applied, it is cleaved by proteases generating a 15 amino acid residues peptide, PnPP-15. PnPP-15 showed an antinociceptive effect in neuropathic pain developed by streptozotocin-induced diabetic mice. The present work aimed to investigate if PnPP-15 is also effective against the inflammatory pain induced by PGE₂. We also evaluated its cytotoxicity <em>in vitro</em> and studied its possible action mechanism in the pain pathway.</p></div><div><h3>Methods</h3><p>The nociceptive threshold was assessed using the mechanical paw pressure test. Paw tissue was collected for protein extraction and western blot analyses. The FRET enzymatic assay measured neprilysin activity. The two-electrode voltage clamp technique measured evoked electrical currents in <em>Xenopus laevis</em> oocytes. Cytotoxicity was measured using multiple cell lines.</p></div><div><h3>Results</h3><p>PnPP-15 has peripheral antinociceptive activity <em>via</em> µ-opioid and CB₁ cannabinoid receptors and inhibits neprilysin. In addition, it induced direct activation of mu-opioid receptors expressed in <em>Xenopus laevis</em> oocytes. PnPP-15 was not cytotoxic against mammalian kidney, liver, heart, nerve, or lung cells.</p></div><div><h3>Conclusion</h3><p>This work demonstrated the antinociceptive effect of PnPP-15 in an inflammatory pain model, suggesting its use as a possible tool for developing new analgesic drugs.</p></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100012"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950200424000120/pdfft?md5=894719be290c29f9baee9c6b92b49796&pid=1-s2.0-S2950200424000120-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141484179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mirabegron alleviates fructose induced nonalcoholic fatty liver disease in rats: Insights into the underlying mechanisms","authors":"Chandaka Madhavarao ,&nbsp;Masa Amala ,&nbsp;Grandhi Sandeep Ganesh","doi":"10.1016/j.prerep.2024.100018","DOIUrl":"10.1016/j.prerep.2024.100018","url":null,"abstract":"<div><h3>Aim</h3><p>Non-alcoholic fatty liver disease (NAFLD) is one of the progressive and chronic disease encompass a range of conditions such as non-alcoholic steatohepatitis (NASH) and cirrhosis. The present study is aimed to elucidate the possible actions of mirabegron, a β3-adrenoreceptor agonist used in the treatment of over active bladder, against NAFLD induced by fructose.</p></div><div><h3>Method</h3><p>30 male Wistar rats were randomized into 5 groups (A) Veh, (B) Fru, (C) Fru + Sita, (D) Fru + Mira and (E) Fru + Mira + Resv. Rats of respective groups were treated with mirabegron (10 mg/kg, p.o.), sitagliptin (10 mg/kg, p.o.) and resveratrol (20 mg/kg, p.o.) daily for 14 days. Fructose water was given to all rats to induce NAFLD till end of the study. Simultaneously, biochemical analysis such as glucose, SGOT, SGPT, HDL, LDL, TC and TG were performed to assess the disease progression. In the end of study hepatic biochemistry, SOD, MDA, GSH, inflammatory markers such as TNF-α, IL-1β and Hematoxylin and Eosin (H&amp;E) analysis were performed.</p></div><div><h3>Key findings</h3><p>The NAFLD rats exhibited a significant weight gain, substantial increase in liver enzymes, glucose, circulating and hepatic total cholesterol, triglycerides, inflammatory cytokines and histological analysis showed hepatic steatosis and inflammation in the Fru group. In contrast, mirabegron alone and in combination with antioxidant provided a promising data on ameliorative effect on hepatic inflammation and steatosis caused by fructose. As a result, mirabegron is found to be a promising therapeutic treatment strategy for NAFLD and its associated complications.</p></div><div><h3>Significance</h3><p>Collectively, findings in this present study revealed that mirabegron reversed NAFLD by suppressing fructose mediated inflammation, oxidative stress and steatosis.</p></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100018"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950200424000181/pdfft?md5=c7adf0763458b6d5f27a71bcab129149&pid=1-s2.0-S2950200424000181-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142149550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reno-protective effect of Roflumilast against kidney injury induced by ischemia/reperfusion in rats: Evidence from biochemical and histological investigations","authors":"Rehab F. Abdel-Rahman ,&nbsp;Marawan A. Elbaset ,&nbsp;Hany M. Fayed ,&nbsp;Tuba Esatbeyoglu ,&nbsp;Sherif M. Afifi ,&nbsp;Rehab Adel Diab","doi":"10.1016/j.prerep.2024.100014","DOIUrl":"10.1016/j.prerep.2024.100014","url":null,"abstract":"<div><p>Oxidative stress, inflammation, and apoptosis are major contributors to renal ischemia/reperfusion (I/R) injury. This study aimed to investigate the effects of pretreatment with the PDE4 inhibitor roflumilast (Rof) on renal I/R and its underlying mechanisms. Sprague-Dawley rats were subjected to 30 minutes of unilateral renal ischemia followed by 45 minutes of reperfusion. Rof (1.5 and 3 mg/kg) was administered for seven days prior to I/R induction. The findings showed that Rof significantly and dose-dependently attenuated kidney damage by reducing blood urea nitrogen and creatinine levels. Rof also exhibited antioxidant and anti-inflammatory effects, as evidenced by improved glutathione and malondialdehyde levels and decreased proinflammatory cytokines (IL-6 and TNF-α). Furthermore, Rof prevented the downregulation of HO-1 and Nrf2 expression. These results suggest that Rof therapy could protect the kidneys from I/R-induced injury through its antioxidant and anti-inflammatory properties, providing a potential therapeutic approach for the management of renal I/R damage.</p></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100014"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950200424000144/pdfft?md5=a3f31ca1c43526d3422212ed0c38e78f&pid=1-s2.0-S2950200424000144-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141962135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in mesenchymal stem cell therapy and natural antioxidants for hepatic fibrosis: A comprehensive review","authors":"Abeer Kazmi ,&nbsp;Tahira Sultana","doi":"10.1016/j.prerep.2024.100016","DOIUrl":"10.1016/j.prerep.2024.100016","url":null,"abstract":"<div><p>Liver damage resulting from the administration of various allopathic drugs and their associated toxicity has become a major health problem, leading to hepatic fibrosis, cirrhosis, and metabolic disorders. This epidemic condition of liver disease represents a major global cause of death and morbidity. Although orthotopic liver transplantation remains a vital treatment option for fibrotic liver conditions, its efficacy is limited by organ scarcity and the risk of immunological rejection. Consequently, alternative therapeutic approaches are urgently needed. Cell-based therapy utilizing mesenchymal stem cells (MSCs) has garnered considerable interest as a promising treatment modality. MSCs exhibit immunomodulatory properties and can differentiate into hepatocytes, thus facilitating the regeneration of damaged hepatocytes and increasing residual hepatocyte proliferation while inhibiting activation or apoptosis of liver stellate cells. However, despite their potential benefits, transplanted cells often exhibit low survival rates due to inadequate oxidative and inflammatory stress resistance. Plants harbor a diverse array of bioactive compounds known to possess hepatoprotective and antioxidant properties. Nanomaterials play a crucial role in regenerative medicine by providing targeted delivery of therapeutic agents and scaffolds for tissue engineering. In treating fibrotic liver, nanomaterials can help mitigate fibrosis progression and promote liver regeneration through controlled release of anti-fibrotic agents and growth factors. This review highlights the synergistic potential of stem cell-based therapy, natural antioxidants, differentiation factors, and nanotechnology in combating hepatic fibrosis and advancing liver regenerative medicine. These combined approaches offer promising avenues for effectively treating fibrotic liver conditions and promoting tissue regeneration.</p></div>","PeriodicalId":101015,"journal":{"name":"Pharmacological Research - Reports","volume":"2 ","pages":"Article 100016"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950200424000168/pdfft?md5=56f9f80a84bc75af31ab28a7294941c3&pid=1-s2.0-S2950200424000168-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}