Shen Yang, Yang Fan, Peng Haiyan, Zhang Guangji, Zhu Fangfang, Xu Haojun, Shi Le
Nanjing Medical University, Nanjing, Jiangsu, China; College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Department of Histology and Embryology, Medical College, Yangzhou University, Yangzhou, Jiangsu, China.
J Ethnopharmacol. 2022 Jan 10;282:114601. doi: 10.1016/j.jep.2021.114601. Epub 2021 Sep 4.
Yanggan Huayu granule (YGHY) is a formula of traditional Chinese medicine that has been widely used to treat patients with liver cancer. But its working mechanism is still poorly understood.
To investigate the anti-tumor effect of YGHY and its working mechanisms in hepatocellular carcinoma (HCC).
H22 mouse xenograft model was used to detect the effect of YGHY on hepatocellular carcinoma (HCC). MTT and CCK8 assays were performed to assess the effect of YGHY on HCC cell growth. Transwell assay was performed to detect the invasion and migration activities of HCC cells. Effect of YGHY drug-contained serum on apoptosis was detected by flow cytometry. Western blot was performed to detect the protein expressions.
Results showed that YGHY inhibited tumor volume and weight, induced the apoptosis of HepG2 and SMMC-7721 cells and increased the protein expressions of Cleaved-Caspase3 and Cleaved-PARP. Furthermore, YGHY significantly down-regulated the protein expression of p-AKT. SC79, as an activator of AKT signaling, was able to increase the expression of p-AKT, and regulate the protein expressions of Cleaved-Caspase3, Cleaved-PARP, BCL-2 and BAX. YGHY drug-contained serum negated the protein expression change provided by SC79.
Taken together, this data indicates that YGHY could inhibit HCC growth by inducing apoptosis, operating through AKT signaling.
养肝化瘀颗粒（YGHY）是一种传统中药配方，已被广泛用于治疗肝癌患者。但其作用机制仍不清楚。
研究YGHY对肝细胞癌（HCC）的抗肿瘤作用及其作用机制。
采用H22小鼠异种移植模型检测YGHY对肝细胞癌（HCC）的作用。采用MTT和CCK8法评估YGHY对肝癌细胞生长的影响。采用Transwell法检测肝癌细胞的侵袭和迁移活性。采用流式细胞术检测含YGHY药物血清对细胞凋亡的影响。采用蛋白质免疫印迹法检测蛋白表达。
结果显示，YGHY可抑制肿瘤体积和重量，诱导HepG2和SMMC-7721细胞凋亡，并增加Cleaved-Caspase3和Cleaved-PARP的蛋白表达。此外，YGHY显著下调p-AKT的蛋白表达。SC79作为AKT信号通路的激活剂，能够增加p-AKT的表达，并调节Cleaved-Caspase3、Cleaved-PARP、BCL-2和BAX的蛋白表达。含YGHY药物血清可抵消SC79引起的蛋白表达变化。
综上所述，这些数据表明YGHY可通过诱导凋亡、经由AKT信号通路发挥作用来抑制肝癌生长。
