Genistein and/or sulfasalazine ameliorate acetic acid-induced ulcerative colitis in rats via modulating INF-γ/JAK1/STAT1/IRF-1, TLR-4/NF-κB/IL-6, and JAK2/STAT3/COX-2 crosstalk

Elhefnawy, Esraa A.; Zaki, Hala F.; El Maraghy, Nabila N.; Ahmed, Kawkab A.; Abd El-Haleim, Enas A.

doi:10.1016/j.bcp.2023.115673

Cited by 9 publications

(3 citation statements)

References 76 publications

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“… 237 The combination of Genistein and Sulfasalazine has an augmented and remarkable effect against oxidative stress and cell apoptosis, over either drug alone. 238 Polysaccharides from eggs of Strongylocentrotus nudus could inhibit the PI3K/protein kinase B(AKT)/mTOR pathway to mediate cytoprotective autophagy by acting on CD36 for alleviating IBD. 239 Hydroxysafflor yellow A, a chalcone glycoside isolated from safflower has been found to ameliorate DSS-induced colitis mice via suppressing pyroptosis by blocking hexokinase 1/NLRP3/gasdermin D pathway and regulating intestinal microbiota.…”

Section: Ibd Treatments: Based On Experimentsmentioning

confidence: 99%

Research advancements and perspectives of inflammatory bowel disease: A comprehensive review

Bai,

Wang,

et al. 2024

Science Progress

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Inflammatory bowel disease (IBD) is a chronic inflammatory disease with increasing incidence, such as Crohn's disease and ulcerative colitis. The accurate etiology and pathogenesis of IBD remain unclear, and it is generally believed that it is related to genetic susceptibility, gut microbiota, environmental factors, immunological abnormalities, and potentially other factors. Currently, the mainstream therapeutic drugs are amino salicylic acid agents, corticosteroids, immunomodulators, and biological agents, but the remission rates do not surpass 30–60% of patients in a real-life setting. As a consequence, there are many studies focusing on emerging drugs and bioactive ingredients that have higher efficacy and long-term safety for achieving complete deep healing. This article begins with a review of the latest, systematic, and credible summaries of the pathogenesis of IBD. In addition, we provide a summary of the current treatments and drugs for IBD. Finally, we focus on the therapeutic effects of emerging drugs such as microRNAs and lncRNAs, nanoparticles-mediated drugs and natural products on IBD and their mechanisms of action.

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Section: Ibd Treatments: Based On Experimentsmentioning

confidence: 99%

Research advancements and perspectives of inflammatory bowel disease: A comprehensive review

Bai,

Wang,

et al. 2024

Science Progress

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“…Due to the complex effects of Axl in IA, R428 treatment inhibits AXL activation in LPS/IFN-g-primed THP-1 cells, but human primary M1 macrophages in vitro did not provide additional translational evidences ( 11 ). In inflammatory diseases, the INF-γ-induced STAT1 signaling contributed to downstream transcription targets activation and oxidative stress ( 137 , 138 ). Of note, this mechanism is also observed in the pro-inflammatory macrophages of IA lesion ( 96 ).…”

Section: Macrophages Relevant Signaling Pathways and Therapy Strategi...mentioning

confidence: 99%

Current understanding of macrophages in intracranial aneurysm: relevant etiological manifestations, signaling modulation and therapeutic strategies

Duan,

Zhao,

et al. 2024

Front. Immunol.

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Macrophages activation and inflammatory response play crucial roles in intracranial aneurysm (IA) formation and progression. The outcome of ruptured IA is considerably poor, and the mechanisms that trigger IA progression and rupture remain to be clarified, thereby developing effective therapy to prevent subarachnoid hemorrhage (SAH) become difficult. Recently, climbing evidences have been expanding our understanding of the macrophages relevant IA pathogenesis, such as immune cells population, inflammatory activation, intra-/inter-cellular signaling transductions and drug administration responses. Crosstalk between macrophages disorder, inflammation and cellular signaling transduction aggravates the devastating consequences of IA. Illustrating the pros and cons mechanisms of macrophages in IA progression are expected to achieve more efficient treatment interventions. In this review, we summarized the current advanced knowledge of macrophages activation, infiltration, polarization and inflammatory responses in IA occurrence and development, as well as the most relevant NF-κB, signal transducer and activator of transcription 1 (STAT1) and Toll-Like Receptor 4 (TLR4) regulatory signaling modulation. The understanding of macrophages regulatory mechanisms is important for IA patients’ clinical outcomes. Gaining insight into the macrophages regulation potentially contributes to more precise IA interventions and will also greatly facilitate the development of novel medical therapy.

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“…As severe and chronic inflammation diseases, the sustained overproduction of inflammatory cytokines like IFN‐γ, TNF‐α, IL‐1β, IL‐6, [10–12] plays a pivotal role as cell‐signaling molecules driving the pathogenesis of UC. Increased production of IL‐6 has been observed in serum and tissue biopsies from human or experimental UC studies and positively correlates with the severity of UC [13,14] .…”

Section: Introductionmentioning

confidence: 99%

Discovery of 6‐Acylamino/Sulfonamido Benzoxazolone with IL‐6 Inhibitory Activity as Promising Therapeutic Agents for Ulcerative Colitis

Ge,

Song,

Cao

et al. 2024

Chemistry & Biodiversity

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Ulcerative colitis has been widely concerned for its persistent upward trend and sustained overproduction of pro‐inflammatory cytokines such as IL‐6 remains a crucial factor in UC development. Therefore, identification of new effective drugs to block inflammatory responses is an urgent and viable strategy for UC. In our research, twenty‐three 6‐acylamino/sulfonamido benzoxazolone derivatives were synthesized, characterized, and evaluated for anti‐inflammatory activity against NO and IL‐6 in LPS‐induced RAW264.7 cells. The results demonstrated that most of the target compounds were capable of reducing the overexpression of NO and IL‐6 to a certain degree. For the most active compounds 3i, 3j and 3l, the inhibitory activities were superior or equivalent to those of the positive drug celecoxib with a dose‐dependent relationship. Furthermore, animal experiments revealed that compounds 3i, 3j and 3l exhibited definitive effect on DSS induced ulcerative colitis by mitigating weight loss and DAI score while decreasing levels of pro‐inflammatory cytokines such as IL‐6 and IFN‐γ, simultaneously increasing production of anti‐inflammatory cytokines IL‐10. Additionally, compounds 3i, 3j and 3l could inhibit oxidative stress to alleviate ulcerative colitis by decreasing MDA and MPO levels. These finding demonstrated that compounds 3i, 3j and 3l hold significant potential as novel therapeutic agents for ulcerative colitis.

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Genistein and/or sulfasalazine ameliorate acetic acid-induced ulcerative colitis in rats via modulating INF-γ/JAK1/STAT1/IRF-1, TLR-4/NF-κB/IL-6, and JAK2/STAT3/COX-2 crosstalk

Cited by 9 publications

References 76 publications

Research advancements and perspectives of inflammatory bowel disease: A comprehensive review

Research advancements and perspectives of inflammatory bowel disease: A comprehensive review

Current understanding of macrophages in intracranial aneurysm: relevant etiological manifestations, signaling modulation and therapeutic strategies

Discovery of 6‐Acylamino/Sulfonamido Benzoxazolone with IL‐6 Inhibitory Activity as Promising Therapeutic Agents for Ulcerative Colitis

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