Song Xiaoqing, Wang Jinying, Zhang Yu, Du Xinqian, Qian Qibing
Basic Medical College of Hebei North University, Zhangjiakou 075000, China.
Chin Herb Med. 2022 Dec 16;15(1):86-93. doi: 10.1016/j.chmed.2022.06.011. eCollection 2023 Jan.
To examine the protective effects of hydroxysafflor yellow A (HSYA) against the senescence of mesenchymal stem cells (MSCs) induced by -galactose (-gal) , and investigate the potential mechanism involved.
Grouping experiment, Normal control (NC) group: conventional culture with complete medium; Senescence group: MSCs were cultured for 48 h with complete medium containing 10 g/L -gal; HSYA group: on the basis of senescence induction, HSYA with the suitable concentration was used to protect MSCs. The key experimental indices associated with oxidative stress, inflammatory response, cell senescence, proliferation and apoptosis were measured through chemical colorimetry, β-galactosidase staining, EdU incorporation and flow cytometry, respectively. The relative quantity (RQ) of proteins related closely to cell proliferation, apoptosis, and NF-κB signaling were measured by Western blotting.
As compared with Senescence group, treatment with HSYA (120 mg/L) effectively ameliorated the adverse situation of MSCs. Oxidation stress and inflammation along with -Gal induction was dramatically alleviated in MSCs; The β-Gal-positive staining indicated that MSC senescence was significantly mitigated; The proliferative capability of MSCs was significantly increased by up-regulating PCNA and inhibiting p16 expression; The anti-apoptotic effect on MSCs was exerted by down-regulating the RQ of cleaved Caspase-3 and Bax; The activity of NF-κB signaling in MSCs was notably suppressed through inhibiting phosphorylation of IKKβ and p65.
HSYA (120 mg/L) significantly delayed the -Gal-induced senescence process in MSCs through attenuating inflammatory reaction and oxidative stress, and suppressing the activity of NF-κB signaling.
研究羟基红花黄色素A（HSYA）对β-半乳糖（β-gal）诱导的间充质干细胞（MSCs）衰老的保护作用，并探讨其潜在机制。
分组实验，正常对照组（NC组）：用完全培养基常规培养；衰老组：将MSCs在含10 g/L β-gal的完全培养基中培养48 h；HSYA组：在诱导衰老的基础上，用合适浓度的HSYA保护MSCs。分别通过化学比色法、β-半乳糖苷酶染色、EdU掺入法和流式细胞术检测与氧化应激、炎症反应、细胞衰老、增殖和凋亡相关的关键实验指标。通过蛋白质印迹法检测与细胞增殖、凋亡和NF-κB信号通路密切相关的蛋白质的相对含量（RQ）。
与衰老组相比，HSYA（120 mg/L）处理有效改善了MSCs的不良状况。MSCs中β-gal诱导的氧化应激和炎症明显减轻；β-Gal阳性染色表明MSCs衰老明显减轻；通过上调PCNA和抑制p16表达，显著提高了MSCs的增殖能力；通过下调裂解的Caspase-3和Bax的RQ，对MSCs发挥抗凋亡作用；通过抑制IKKβ和p65的磷酸化，显著抑制了MSCs中NF-κB信号通路的活性。
HSYA（120 mg/L）通过减轻炎症反应和氧化应激，抑制NF-κB信号通路的活性，显著延缓了β-gal诱导的MSCs衰老过程。
