We proposed a novel strategy in the fabrication of biodegradable poly(acrylic acid-co-acrylamide)/poly(vinyl alcohol) (P(AAc-co-Am)/PVA) double network (DN) hydrogels with good mechanical and self-healing properties. In the DN hydrogel system, P(AAc-co-Am) polymers form a network through the ionic coordinates between –COO– and Fe3+ and hydrogen bonding between –COOH and –CONH2, while another network is fabricated by the complexation between PVA and borax. The influences of the composition on the rheological behaviors and mechanical properties of the synthesized DN hydrogels were investigated. The rheological measurements revealed that the viscoelasticity and stiffness of the P(AAc-co-Am)/PVA DN hydrogels increase as the acrylamide and Fe3+ concentrations increase. At 0.05 mmol of Fe3+ and 50% of acrylamide, tensile strength and elongation at break of P(AAc-co-Am)/PVA DN hydrogels could reach 329.5 KPa and 12.9 mm/mm, respectively. These properties arise from the dynamic reversible bonds existed in the P(AAc-co-Am)/PVA DN hydrogels. These reversible bonds also give good self-healing properties, and the maximum self-healing efficiency of P(AAc-co-Am)/PVA DN hydrogels is up to 96.4%. The degradation test of synthesized DN hydrogels was also conducted under simulated physiological conditions and the weight loss could reach 74% in the simulated intestinal fluid. According to the results presented here, the synthesized P(AAc-co-Am)/PVA DN hydrogels have a potential application prospect in various biomedical fields.
Glioblastoma multiforme (GBM) is a malignant tumor caused by complex pathological mechanisms, and is characterized by a high rate of cancer-related mortality and poor patient prognosis. Overgrowth of cancer cells, which results from the inhibition of cell apoptosis and/or the promotion of cell proliferation, leads to the progression of GBM. Therefore, studies into the regulatory mechanisms of cancer cell growth in GBM are required to identify potential therapeutic targets and improve treatment for GBM. In the present study, the role of insulin-like growth factor 1 (IGF1)/IGF1 receptor (IGF1R) signaling in the survival of GBM cells was evaluated. It was observed that IGF1 significantly inhibited the intrinsic and extrinsic pathways of apoptosis (P<0.05), and overexpression of IGF1R significantly promoted the survival of GBM cells (P<0.05). Moreover, both exogenous IGF1 and overexpression of IGF1R promoted the phosphorylation of protein kinase B (AKT), and inhibition of the phosphoinositide 3-kinase (PI3K)/AKT pathway significantly attenuated the inhibitory effects of IGF1/IGF1R on GBM apoptosis (P<0.05). Collectively, these findings indicate that IGF1/IGF1R promotes the survival of GBM cells through activation of the PI3K/AKT pathway. Therefore, inhibition of IGF1/IGF1R may be a viable therapeutic strategy to suppress the progression of GBM.
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