Kunming Key Laboratory of Stem Cell and Regenerative Medicine, 920th Hospital of the PLA Joint Logistics Support Force, Kunming, 650032, Yunnan Province, China.
Stem Cells and Immune Cells Biomedical Techniques Integrated Engineering Laboratory of State and Regions, 920th Hospital of the PLA Joint Logistics Support Force, Kunming, 650032, Yunnan Province, China.
Stem Cell Res Ther. 2021 Mar 1;12(1):156. doi: 10.1186/s13287-021-02201-3.
Age-associated lung tissue degeneration is a risk factor for lung injury and exacerbated lung disease. It is also the main risk factor for chronic lung diseases (such as COPD, idiopathic pulmonary fibrosis, cancer, among others). So, it is particularly important to find new anti-aging treatments.
We systematically screened and evaluated elderly senile multiple organ dysfunction macaque models to determine whether BMMSCs inhibited lung tissue degeneration.
The average alveolar area, mean linear intercept (MLI), and fibrosis area in the elderly macaque models were significantly larger than in young rhesus monkeys (p < 0.05), while the capillary density around the alveoli was significantly low than in young macaque models (p < 0.05). Intravenous infusion of BMMSCs reduced the degree of pulmonary fibrosis, increased the density of capillaries around the alveoli (p < 0.05), and the number of type II alveolar epithelium in elderly macaques (p < 0.05). In addition, the infusion reduced lung tissue ROS levels, systemic and lung tissue inflammatory levels, and Treg cell ratio in elderly macaque models (p < 0.05). Indirect co-cultivation revealed that BMMSCs suppressed the expression of senescence-associated genes, ROS levels, apoptosis rate of aging type II alveolar epithelial cells (A549 cells), and enhanced their proliferation (p < 0.05).
BMMSC treatment inhibited age-associated lung tissue degeneration.
与年龄相关的肺组织退化是肺损伤和加重肺部疾病的危险因素。它也是慢性肺部疾病（如 COPD、特发性肺纤维化、癌症等）的主要危险因素。因此，寻找新的抗衰老治疗方法尤为重要。
我们系统地筛选和评估了老年衰老多器官功能障碍猕猴模型，以确定 BMMSCs 是否抑制肺组织退化。
老年猕猴模型的平均肺泡面积、平均线性截距（MLI）和纤维化面积明显大于年轻恒河猴（p<0.05），而肺泡周围的毛细血管密度明显低于年轻猕猴模型（p<0.05）。静脉输注 BMMSCs 可降低肺纤维化程度，增加肺泡周围毛细血管密度（p<0.05），增加老年猕猴模型中 II 型肺泡上皮细胞的数量（p<0.05）。此外，输注可降低老年猕猴模型中的肺组织 ROS 水平、全身和肺组织炎症水平以及 Treg 细胞比例（p<0.05）。间接共培养显示，BMMSCs 抑制衰老相关基因的表达、ROS 水平、衰老 II 型肺泡上皮细胞（A549 细胞）的凋亡率，并增强其增殖（p<0.05）。
BMMSC 治疗抑制了与年龄相关的肺组织退化。
