Molecular Biotechnology, Год журнала: 2023, Номер unknown
Опубликована: Ноя. 30, 2023
Язык: Английский
Journal of Reproductive Immunology, Год журнала: 2024, Номер 162, С. 104213 - 104213
Опубликована: Фев. 9, 2024
Endometriosis (EMS) is known to be closely associated with inflammation. We evaluate the possible mechanism linking PI3K/AKT signaling pathway pyroptosis and inflammation in EMS. collected 30 patients undergoing laparoscopic for endometriosis as EMS group those surgery uterine fibroids control group, from whom we serum, normal endometrium, eutopic endometrium ectopic endometrium. Transmission electron microscopy (TEM) was used observe internal structure of endometrial cells. Western Blot detect protein expression PI3K, P-PI3K, AKT, P-AKT, NLRP3, Caspase-1, GSDMD, GSDMD-N. Immunohistochemistry (IHC) staining GSDMD-N proteins. Immunofluorescence (IF) Quantitative real-time polymerase chain reaction (qRT-PCR) analyze mRNA levels ELISA serum IL-1β, IL-18, TLR4, NF-κB. found that activation significantly increased level cellular inflammatory factors. Our results suggest there a positive correlation between pyroptosisas well patients.
Язык: Английский
Процитировано
11
Neurochemistry International, Год журнала: 2024, Номер 175, С. 105676 - 105676
Опубликована: Фев. 7, 2024
Язык: Английский
Процитировано
9
Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(1)
Опубликована: Янв. 1, 2025
ABSTRACT Subarachnoid hemorrhage (SAH) is a specific type of stroke. Dihydroquercetin (DHQ), flavonoid, known for its various pharmacological properties. This study aimed to explore the roles and mechanisms DHQ in influencing progression SAH. A rat SAH model was established using endovascular perforation technique. Following induction, administered orally 1 h later. Assessments included scores, neurological function, brain swelling, blood‐brain barrier (BBB) integrity, neuronal damage, apoptosis levels, inflammation, indicators ferroptosis treatments. The HT22 cells were exposed hemin simulate SAH‐like conditions under vitro settings. Cell counting kit‐8 assays, flow cytometry, enzyme?linked immunosorbent assay, BODIPY 581/591 C11 staining, western blot analysis, biochemical kits employed evaluate potential effects DHQ. Moreover, responsible protective effect examined by analysis. vivo findings revealed that mitigated impairments, BBB disruption, injury at 24 post‐SAH. also reduced degeneration, following enhanced cell survival exposure. Mechanistically, activated phosphatidylinositol‐4,5‐bisphosphate 3‐kinase (PI3K)/protein kinase B (AKT)/nuclear factor erythroid 2‐related 2 (Nrf2) signaling rats hemin‐treated exert neuroprotective effects. In conclusion, this reveals can effectively decrease permeability, edema, dysfunctions, post‐SAH activating PI3K/AKT/Nrf2/HO‐1 pathway.
Язык: Английский
Процитировано
1
Proceedings of the National Academy of Sciences, Год журнала: 2025, Номер 122(11)
Опубликована: Март 11, 2025
Inflammation is among the known causes of cisplatin-induced hearing loss (CIHL), but its exact pathophysiological mechanisms remain unclear. Herein, we demonstrated that pyroptosis—a recently identified inflammatory type regulated cell death dependent on gasdermin D (GSDMD)—was activated in cochleae cisplatin-treated mice, causing CIHL. Meanwhile, treatment with GSDMD inhibitor necrosulfonamide alleviated CIHL these mice. To further examine role GSDMD-mediated pyroptosis CIHL, conducted experiments Gsdmd- deficient mice . Gsdmd −/− significantly lower cochlear damage than control and appeared to be invulnerable Furthermore, stria vascularis (SV), not hair cells (HCs), played a dominant In marginal (MCs) SV, cisplatin induced caspase-dependent cleavage, pore-forming N-terminal rapidly localized mitochondria, leading abnormal mitochondrial aggregation oxidative stress. The consequent dysfunction MCs might result severe progression inflammation, SV damage, HC loss. Notably, pharmacological inhibition using FDA-approved drug disulfiram effectively symptoms Collectively, findings offer broad avenue for inhibiting pyroptosis-induced ototoxicity provide valuable theoretical insights clinical management
Язык: Английский
Процитировано
1
Molecular Neurobiology, Год журнала: 2024, Номер 61(12), С. 10271 - 10287
Опубликована: Май 7, 2024
Язык: Английский
Процитировано
7
Pharmacological Research, Год журнала: 2024, Номер 201, С. 107089 - 107089
Опубликована: Янв. 29, 2024
Chronic pain has been proven to be an independent disease, other than accompanying symptom of certain diseases. Interleukin-18 (IL-18), a pro-inflammatory cytokine with pleiotropic biological effects, participates in immune modulation, inflammatory response, tumor growth, as well the process chronic pain. Compelling evidence suggests that IL-18 is upregulated occurrence Antagonism or inhibition expression can alleviate and development And located microglia, while IL-18R mostly astrocytes spinal cord. This indicates interaction between microglia mediated by IL-18/IL-18R axis involved In this review, we described role mechanism different types review provides strong potential therapeutic target management.
Язык: Английский
Процитировано
5
Molecular Neurobiology, Год журнала: 2024, Номер 61(10), С. 8051 - 8068
Опубликована: Март 9, 2024
Язык: Английский
Процитировано
5
Experimental Neurology, Год журнала: 2024, Номер 383, С. 115043 - 115043
Опубликована: Ноя. 8, 2024
Язык: Английский
Процитировано
4
Brain Disorders, Год журнала: 2025, Номер 17, С. 100203 - 100203
Опубликована: Фев. 21, 2025
Язык: Английский
Процитировано
0
Inflammopharmacology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 26, 2025
Spinal cord injury (SCI), which is characterized by motor and/or sensory dysfunction, presents a significant health challenge resulting from mechanical trauma. Secondary injury, follows the trauma and driven factors such as inflammation, plays critical role in SCI pathophysiology. Scientific evidence indicates that treatment strategies aimed at modulating inflammation during acute phase of alleviate seconder injury. In this regard, present study seeks to evaluate effectiveness certolizumab, monoclonal antibody targeting TNF-α widely used various inflammatory diseases, model. study, Control, Trauma, Trauma + Certolizumab groups were established, each comprising eight male rats. One hour after induction, rats group administered 10 µg dissolved saline intraperitoneally, while Control received an equivalent volume saline. After Modified Tarlov Scoring was performed on seventh day experiment, all sacrificed. The effects certolizumab neuroinflammation apoptosis model evaluated using histological, biochemical, molecular analyses blood tissue samples obtained downregulated expression TNF-α, NF-κB, IL-6. addition, evidenced TUNEL assay, Caspase-3 (an apoptotic marker), Score results, effectively suppressed inflammation-induced neural alleviated locomotor deficits. exerts neuroprotective effect against secondary damage through inhibition apoptosis.
Язык: Английский
Процитировано
0