인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Steroid-induced osteonecrosis of the femoral head (SIONFH) is a debilitating orthopedic condition. This study investigated the mechanism of Tanshinone I (TsI) in SIONFH modulating apoptosis in SIONFH via the PI3K/AKT/mTOR pathway. A SIONFH rat model was treated with TsI and a PI3K activator. Bone mineral density (BMD), bone volume/total volume (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), and trabecular separation (Tb.Sp) were determined by microCT. Empty lacunae count, Osteopontin, and apoptosis of the femoral head tissues were assessed. Levels of Bax, cleaved-caspase-3, Bcl-2, and AKT, PI3K, and mTOR phosphorylation in femoral head tissues were determined by Western blot. SIONFH rats exhibited decreased BMD, BV/TV, Tb.N, and Tb.Th, increased Tb.Sp, reduced Osteopontin-positive cells, increased empty lacunae rate, and TUNEL and Osteopontin co-positive cells, elevated Bax and cleaved-caspase-3 protein levels, and diminished Bcl-2 protein expression. TsI promoted osteogenesis, attenuated SIONFH, and reduced apoptosis in SIONFH rats. TsI inhibited AKT, PI3K, and mTOR phosphorylation levels in the femoral head tissues of SIONFH rats, thereby repressing the PI3K/AKT/mTOR pathway activation. Activating the PI3K/AKT/mTOR pathway partially reversed TsI's effect in rats. Collectively, TsI limited the PI3K/AKT/mTOR pathway activation to reduce osteocyte apoptosis in SIONFH rats, which provided potential therapeutic insights for SIONFH treatment.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.