Machihara Kayo, Oki Shoma, Maejima Yuka, Kageyama Sou, Onda Ayumu, Koseki Yurino, Imai Yasuyuki, Namba Takushi
Research and Education Faculty, Multidisciplinary Science Cluster, Interdisciplinary Science Unit, Kochi University, Kochi 783-8505, Japan.
Department of Marine Resource Science, Faculty of Agriculture and Marine Science, Kochi University, Kochi 783-8502, Japan.
iScience. 2023 Jun 14;26(7):107113. doi: 10.1016/j.isci.2023.107113. eCollection 2023 Jul 21.
Reactive oxygen species (ROS), such as superoxide, are crucial factors involved in the stimulation of cellular aging. Mitochondria, which are important organelles responsible for various metabolic processes in cells, produce ROS. These ROS impair mitochondrial function, thereby accelerating aging-related cellular dysfunction. Herein, we demonstrated that the polysaccharide complex (SPC) restores mitochondrial function and collagen production by scavenging superoxide via the upregulation of superoxide dismutase 2 (SOD2) in aging fibroblasts. We observed that SOD2 expression was linked to inflammatory pathways; however, SPC did not upregulate the expression of most inflammatory cytokines produced as a result of induction of LPS in aging fibroblasts, indicating that SPC induces SOD2 without activation of inflammatory pathways. Furthermore, SPC stimulated endoplasmic reticulum (ER) protein folding by upregulating ER chaperones expression. Thus, SPC is proposed to be an antiaging material that rejuvenates aging fibroblasts by increasing their antioxidant potential via the upregulation of SOD2.
活性氧（ROS），如超氧化物，是刺激细胞衰老的关键因素。线粒体作为细胞内负责各种代谢过程的重要细胞器，会产生ROS。这些ROS会损害线粒体功能，从而加速与衰老相关的细胞功能障碍。在此，我们证明了多糖复合物（SPC）通过上调衰老成纤维细胞中超氧化物歧化酶2（SOD2）来清除超氧化物，从而恢复线粒体功能和胶原蛋白生成。我们观察到SOD2的表达与炎症途径相关；然而，SPC并未上调衰老成纤维细胞中因脂多糖诱导而产生的大多数炎性细胞因子的表达，这表明SPC在不激活炎症途径的情况下诱导SOD2。此外，SPC通过上调内质网伴侣蛋白的表达来刺激内质网（ER）蛋白折叠。因此，SPC被认为是一种抗衰老物质，它通过上调SOD2来增加衰老成纤维细胞的抗氧化能力，从而使其恢复活力。
