Yazar "Jalili-Nik, Mohammad" seçeneğine göre listele

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    Curcumin as a modulator of IL-18: A promising therapeutic approach for inflammatory diseases
    (Elsevier, 2026) Kaviani, Maryam; Ghoflchi, Sahar; Disfani, Saba Miri; Jalili-Nik, Mohammad; Sadeghi, Asie; Karav, Sercan; Kesharwani, Prashant
    Inflammatory and immune-related pathways act as a central mediator in the pathogenesis of a wide range of diseases, including cancer, cardiovascular diseases, kidney disorders, acute lung injury, autoimmune conditions, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. The activation of the NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome, a key component of innate immunity, promotes inflammation through the release of interleukin (IL)-18. By enhancing the production of other pro-inflammatory cytokines like interferon (IFN)-gamma and facilitating T-helper cell polarization, IL-18 amplifies the inflammatory cascade. Research indicates that curcumin effectively suppresses IL-18 production and modulates signaling pathways that contribute to its activation, including the nuclear factor kappa B (NF-kappa B) and NLRP3 inflammasome pathways. NF-kappa B, a master regulator of inflammation, is directly influenced by curcumin, which inhibits its translocation to the nucleus, thereby downregulating the expression of IL-18 and other inflammatory mediators. By targeting upstream regulators and components of the inflammasome, curcumin reduces pyroptosis, oxidative stress, and cytokine storm-like responses, offering a multifaceted therapeutic approach. The role of curcumin in modulating oxidative stress and immune responses positions it as a promising adjunct or alternative therapeutic agent for diseases linked to IL-18 dysregulation. Preclinical and clinical studies have further demonstrated synergistic effects when combined with conventional therapies. This highlights its potential not only in mitigating disease progression but also in addressing underlying inflammatory processes such as chronic inflammatory disease, cardiovascular disease, and neurodegenerative disease. Given these attributes, targeting IL-18 with curcumin-based interventions is the way for novel therapeutic strategies that balance efficacy with minimal side effects, addressing both symptoms and underlying disease mechanisms.
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    Harnessing the role of insulin-like growth factor in glioblastoma: a comprehensive review
    (Pergamon-Elsevier Science Ltd, 2026) Nakhaei, Ali; Afshari, Sadaf; Mohammadian, Mohammad; Ahmadi, Seyed Sajad; Mohatshami, Elmira; Jalili-Nik, Mohammad; Jalali, Mahsa
    This review provides an overview of the biological function of the insulin-like growth factor (IGF) system in glioblastoma (GB) development and a thorough examination of its therapeutic relevance. Networks of micro-RNAs regulated by insulin-like growth factor 1 (IGF-1) that impede GB's response to temozolomide (TMZ). The amounts of PDGFR, IGF1R, PI3K, and ERK1/2 proteins and their potential as therapeutic targets. Anti-epidermal growth factor receptor (EGFR) agents may encounter significant resistance from IGF-R inhibitors that operate via PI3K signaling pathways. Insulin-like growth factor-binding protein (IGFBP)-2 modulates CD24, hence increasing the invasiveness of GB cells. 5) Due to the proliferation, invasion, and chemotherapy resistance of GB cells when exposed to exogenous IGFBP-2, targeting the integrin beta 1/ERK signaling pathway may serve as an effective therapeutic strategy for GB treatment. The IGFBP-2/integrin/ILK/NF-kappa B network functions as a biologically active signaling pathway in vivo, facilitating the proliferation of GB. Activation of the Hedgehog (HH) pathway and overexpression of the downstream effector GLII accelerate glioma tumorigenicity and the biology of glioma stem cells (GSCs). The aggressive nature of gliomas is attributed to PTEN failure and elevated levels of IGFBP-2 expression. IGFBP-2 augments the expression of CD144 and MMP2, promoting the development of vasculogenic mimicry (VM) in GB cells. Recent investigations have revealed a crucial signaling mechanism that is vital for the survival of GB patients.
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    Repurposing ivermectin: a new hope for glioblastoma multiforme?
    (Springer Birkhauser, 2025) Mohtashami, Elmira; Bibak, Bahram; Sanati, Mehdi; Afshari, Sadaf; Kahkhaie, Kolsoum Rezaie; Vahedi, Mohammad Mahdi; Jalili-Nik, Mohammad; Karav, Sercan
    Ivermectin is the most extensively researched macrocyclic lactone due to its potential anticancer and antiparasitic use. Nonetheless, there are more compounds within this family, including doramectin and abamectin. In the current era of medicinal repurposing, ivermectin has received renewed focus following its initial development for the treatment of parasitic conditions such as scabies, elephantiasis, and river blindness. Recent studies indicate that ivermectin may inhibit the proliferation of specific tumor cells by regulating many signaling pathways implicated in cancer progression. Despite the growing body of research on the topic, critical issues about its anticancer processes remain unresolved. Our study focused on ivermectin, its mechanisms of action, and its potential uses against glioblastoma multiforme (GBM).
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    SGLT-2 inhibitors beyond diabetes: a new frontier in cancer treatment
    (Elsevier Ireland Ltd, 2025) Nakhaei, Ali; Delavar, Kiana; Azim, Azin Sadat; Afshari, Sadaf; Mohtashami, Alireza; Jalili-Nik, Mohammad; Jalali, Mahsa; Karav, Sercan
    Sodium-glucose co-transporter 2 (SGLT-2) inhibitors, a new class of antidiabetic medications including canagliflozin, dapagliflozin, ipragliflozin, and empagliflozin, recently came to light as possible anti-cancer therapeutics. The confirmed presence of SGLT-2 in many cancer cell lines further substantiates their potential as therapeutic targets. Because many cancer cells change their metabolism to become more glucose-dependent, blocking glucose absorption with SGLT-2 inhibitors is an intriguing anti-cancer therapy. In addition to their physiological function in renal proximal tubules, SGLT-2 has been identified in specific tumor cells. Clinical trials have shown that SGLT-2 inhibitors are safe and well-tolerated in individuals with diabetes and heart failure. Significantly, these medicines demonstrate antiproliferative effects across multiple cancer types, as substantiated by both in vitro and in vivo models, frequently via mechanisms that are independent of SGLT-2 itself. They seem to regulate a diverse array of intracellular and extracellular signaling pathways, encompassing those associated with microRNAs, AMPK, ERK, DNA and RNA metabolism, ATP homeostasis, and mitochondrial function. These data collectively underscore the potential of SGLT-2 inhibitors in clinical oncology and elucidate the processes driving their anti-cancer efficacy.