College of Life Science, Northwest Normal University, Lanzhou 730000, China.
College of Life Science, Lanzhou University, Lanzhou 730000, China.
J Tradit Chin Med. 2023 Feb;43(1):87-94. doi: 10.19852/j.cnki.jtcm.2023.01.008.
To investigate the efficacy of Astragaloside IV (AS-IV) on radiation-induced liver inflammation in mice.
The mice were divided into normal group, dimethyl sulfoxide solvent group, irradiation group (IR), irradiation + AS-IV (20 mg/kg) group (IR+AS-20) and irradiation + AS-IV (40 mg/kg) group (IR+AS-40). One month after intraperitoneal injection of AS-IV, the mice were irradiated with 8Gry Co60γ, the blood was collected for biochemical analysis, and the liver was collected for hematoxylin-eosin staining, immunofluorescence and electron microscopic observation, oxidative stress, and Western blot analysis.
The AS-IV treatment significantly ameliorated the pathological morphology of liver and reduced the alanine aminotransferase and aspertate amino-transferase levels in serum induced by radiation; AS-IV treatment also significantly reduced the expression of inflammatory factors tumor necrosis factor alpha and interleukin 6 and antagonized malonaldehyde content and superoxide dismutase activity in liver caused by radiation; in addition, AS-IV treatment can significantly inhibited the positive expression of thioredoxin-interacting protein (TXNIP) and nod-like receptor protein 3 (NLRP3) inflammasome in liver tissue after radiation; The expression of TXNIP, NLRP3 inflammasome, apoptosis-associated speck-like protein containing a CARD, cysteinyl aspartate-specific proteinase 1 and interleukin 1beta in the AS-IV prevention group decreased significantly compared to the radiation group.
These findings suggested that Co60γ radiation can cause structural and functional damage to the liver, which may be related to the NLRP3 mediated inflammatory pathway; AS-IV may play a protective role by inhibiting the TXNIP/NLRP3 inflammasome signaling pathway in the radiation-induced liver injury model.
研究黄芪甲苷（AS-IV）对小鼠放射性肝炎症的疗效。
将小鼠分为正常组、二甲基亚砜溶剂组、照射组（IR）、照射+AS-IV（20mg/kg）组（IR+AS-20）和照射+AS-IV（40mg/kg）组（IR+AS-40）。AS-IV 腹腔注射 1 个月后，用 8Gry Co60γ照射小鼠，采集血液进行生化分析，采集肝脏进行苏木精-伊红染色、免疫荧光和电镜观察、氧化应激和 Western blot 分析。
AS-IV 治疗显著改善了肝脏的病理形态，降低了辐射引起的血清丙氨酸氨基转移酶和天门冬氨酸氨基转移酶水平；AS-IV 治疗还显著降低了炎症因子肿瘤坏死因子-α和白细胞介素 6 的表达，并拮抗了辐射引起的肝丙二醛含量和超氧化物歧化酶活性的增加；此外，AS-IV 治疗可显著抑制辐射后肝组织中硫氧还蛋白相互作用蛋白（TXNIP）和核苷酸结合寡聚结构域样受体蛋白 3（NLRP3）炎性小体的阳性表达；与照射组相比，AS-IV 预防组肝组织中 TXNIP、NLRP3 炎性小体、凋亡相关斑点样蛋白含有 CARD、半胱天冬氨酸特异性蛋白酶 1 和白细胞介素 1β的表达明显降低。
这些发现表明，Co60γ 辐射会导致肝脏结构和功能损伤，这可能与 NLRP3 介导的炎症途径有关；AS-IV 可能通过抑制 TXNIP/NLRP3 炎性小体信号通路在辐射诱导的肝损伤模型中发挥保护作用。
