摘要:
Provided is an artificial eardrum using silk protein and a method of fabricating the same. The artificial eardrum is fabricated in the form of a silk membrane by desalinating and drying silk protein (or silk fibroin) or a silk protein complex solution obtained after removal of sericin from a silkworm cocoon or silk fiber. Thus, regeneration of an eardrum perforated due to disease or a sudden accident is stimulated, a boundary of the regenerated eardrum is clean and biocompatibility and transparency are increased. In addition, the artificial eardrum may be fabricated using the silk protein or silk protein complex solution obtained from a silkworm cocoon alone or mixed with collagen, alginic acid, PEG or pluronic 127.
摘要:
Provided is an artificial eardrum using silk protein and a method of fabricating the same. The artificial eardrum is fabricated in the form of a silk membrane by desalinating and drying silk protein (or silk fibroin) or a silk protein complex solution obtained after removal of sericin from a silkworm cocoon or silk fiber. Thus, regeneration of an eardrum perforated due to disease or a sudden accident is stimulated, a boundary of the regenerated eardrum is clean and biocompatibility and transparency are increased. In addition, the artificial eardrum may be fabricated using the silk protein or silk protein complex solution obtained from a silkworm cocoon alone or mixed with collagen, alginic acid, PEG or pluronic 127.
摘要:
The present invention provides bee venom which can decrease expression levels of sclerotic factors, inflammatory factors and vascular adhesion factors associated with atherosclerosis, and a pharmaceutical composition comprising the bee venom as an active ingredient for the treatment of the atherosclerosis. When the bee venom was administered to laboratory animal models of atherosclerosis, the total cholesterol and neutral lipid were decreased, high-density cholesterol was maintained or even increased, the expression levels of TNF-α and IL-β as inflammation-associated cytokines were decreased in the blood, the expression levels of fibrosis-associated cytokines and vascular adhesion factors were decreased in the main artery and the heart, the plaque deposition generally caused by the atherosclerosis was decreased, and the expression levels of intercellular adhesion molecules (ICAM) and vascular cell adhesion molecules (VCAM), TGF-β1 and fibronectin as fibrosis-related cytokines were decreased.