A Simple and Efficient Method to Improve Mechanical Properties of Collagen Scaffolds by UV Irradiation

Collagen is the major protein component of cartilage, bone, skin and connective tissue and constitutes the major part of the extracellular matrix. Collagen type I has complex structural hierarchy, which consists of treepolypeptide α-chains wound together in a rod-like helical structure. Collagen is an important biomaterial, finding many applications in the field of tissue engineering. It has been processed into various shapes, such as, gel, film, sponge and fiber. It is commonly used as the scaffolding material for tissue engineering due to its many superior properties including low antigenicity and high growth promotion. Unfortunately, poor mechanical properties and rapid degradation rates of collagen scaffolds can cause instability and difficulty in handling. By crosslinking, the structural stability of the collagen and its rate of resorption can be adapted with respect to its demanding requirements. The strength, resorption rate, and biocompatibility of collagenous biomaterials are profoundly influenced by the method and extent of crosslinking. In thisstudy, the effect of UV irradiation on collagen scaffolds has been carried out.Collagen scaffolds were fabricated using freeze drying method with freezing temperature of -80oC, then exposed to UV irradiation. Mean pore size of the scaffolds was obtained as 98.52±14.51 μm using scanning electron microscopy. Collagen scaffolds exposed to UV Irradiation (254 nm) for 15 min showed the highest tensile strain (17.37±0.98 %), modulus (1.67±0.15 MPa) and maximum load (24.47±2.38 cN) values. As partial loss of the native collagen structure may influence attachment, migration, and proliferation of cells on collagen scaffolds, we detected no intact α-chains after SDS-Page chromatography. We demonstrate that UV irradiation is a rapid and easily controlled means of increasing the mechanical strength of collagen scaffolds without any molecular fracture

Increased phosphorylation of mTOR is involved in remote ischemic preconditioning of hippocampus in mice

Different signaling pathways are involved in tissue protection against ischemia reperfusion (IR) injury, among them mammalian target of rapamycin (mTOR) and related pathways have been examined in many recent studies. Present study evaluated the role of mTOR in remote ischemic preconditioning (RIPC) of hippocampus. Renal ischemia was induced (3 cycles of 5 min occlusion and 5 min reperfusion of unilateral renal artery) 24 h before global brain ischemia (20 min bilateral common carotid artery occlusion). Saline or rapamycin (mTOR inhibitor; 5 mg/kg, i.p.) was injected 30 min before RIPC. mTOR and phosphorylated mTOR (p-mTOR) expression, superoxide dismutase (SOD) activity and retention trial of passive avoidance test were determined 24 h after global ischemia. Apoptosis and neuronal cell density were assessed 72 h after hippocampal ischemia. RIPC decreased apoptosis (p<0.05 vs. IR), improved memory (p<0.05 vs. IR), and augmented p-mTOR expression and SOD activity after hippocampal ischemia (p<0.05 vs. IR). Rapamycin abolished all protective effects of RIPC (p<0.05 vs. RIPC+IR) suggesting a role for mTOR in RIPC induced hippocampal protection. © 2013 Elsevier B.V. All rights reserved