In this study, a multifunctional composite hydrogel was developed by combining Sodium Alginate (Alg) with synthesized Poly(propylene glycol) phosphazene (PGP) for infected wound healing. Structural characterizations confirmed successful matrix formation, yielding a tunable macroporous network with excellent swelling capacity, high biosafety (hemolysis <5%), and prominent cell viability exceeding 100% in L929 fibroblasts. Erythromycin (Ery) was efficiently loaded (85.13%) and exhibited a sustained release profile over 96 h. Crucially, the Alg/PGP/Ery composite demonstrated strong synergistic antibacterial and bactericidal efficacy against both S. aureus and E. coli via a membrane-permeabilizing mechanism verified by FESEM. In vivo evaluations in a full-thickness infected rat model confirmed accelerated wound closure (75% y day 14) and marked clearance of the tissue bacterial burden. Furthermore, the hydrogel significantly suppressed local pro-inflammatory cytokine levels (TNF-α and IL-6) while upregulating angiogenic (VEGF) and extracellular matrix (Collagen I) gene expression. Histological examination corroborated superior tissue remodeling with complete re-epithelialization and the regeneration of cutaneous appendages including hair follicles and sebaceous glands. These findings demonstrate that the Alg/PGP/Ery hydrogel holds great promise as an advanced dressing for infected cutaneous wound repair.
Mahnaz Mohammadpour, Faramarz Hamzehpour, Alireza Lotfabadi et al.· International Journal of Bio...· 0 citations
Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. This study aimed to elucidate the dynamic interplay between these pathological pathways in a rotenone-induced rat model of PD. Adult male Wistar rats were chronically treated with rotenone. Behavioral assessments included Rotarod, Open Field, Rotating Pole, and Cylinder tests. On days 7, 14, and 21, gene expression levels of key markers including α-synuclein, NLRP3 inflammasome components (NLRP3, ASC), inflammatory cytokines (IL-1β, TNF-α, IL-6), upstream signaling molecules (TLR4, NF-κB), antioxidant defense factors (Nrf2, HO-1), apoptotic regulators (Bax, Bcl-2, Caspase-3), and tyrosine hydroxylase (TH) were quantified via qPCR. Crucially, protein abundance for all major markers was validated using ELISA, alongside biochemical assessment of oxidative stress markers (MDA and SOD). Rotenone treatment caused a progressive decline in motor performance across all behavioral assays (p < 0.001), including reduced rotarod latency, decreased open field distance, increased pole test latency, and heightened cylinder asymmetry. The PD group exhibited significant time-dependent increases in α-synuclein, TLR4, NF-κB, NLRP3, ASC, IL-1β, IL-6, TNF-α, Bax, Caspase-3, and MDA levels. Conversely, expression levels of Nrf2, HO-1, Bcl-2, and SOD activity showed marked decreases (p < 0.01). Finally, TH expression decreased progressively, reaching roughly 50% of control levels at day 21. Correlation analysis confirmed strong links between α-synuclein accumulation, inflammation, oxidative damage, and neuronal loss. These findings suggest a synergistic pathogenic cascade where α-synuclein accumulation contributes to neuroinflammation and oxidative stress, suppressing antioxidant defenses and activating apoptotic pathways, ultimately leading to dopaminergic neuron death and severe motor dysfunction.
Homa Vali Pour, M. Alfateh, Sanaz Mirzayan Shanjani et al.· Biochemical and Biophysical...· 0 citations
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