Yu Jinhong, Yang Chaofeng, Zhang Pengwei, Wei Min, Li Yang
Sichuan Key Laboratory of Medical Imaging, Department of Ultrasound, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Sichuan Key Laboratory of Medical Imaging, Department of Radiology, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Front Chem. 2025 Apr 4;13:1475026. doi: 10.3389/fchem.2025.1475026. eCollection 2025.
Asialoglycoprotein receptor (ASGPR) is an endocytic C-type lectin receptor in hepatocytes. Acute and chronic liver diseases can result in the decreased expression and content of this receptor. The objective of this study was to determine whether ASGPR-targeted perfluorooctylbromide (PFOB) can enhance ultrasound imaging signals and evaluate the severity of carbon tetrachloride (CCl4)-induced acute liver damage in rats. The specificity of ASGPR-targeted PFOB for hepatocytes L-02 was investigated . , all rats were treated with either ASGPR-targeted PFOB or PFOB, and ultrasound imaging of the livers was performed to evaluate the effect of these treatments on the imaging signal. The effects of CCl4 injection were also examined by measuring the percentage of apoptotic hepatocytes and ASGPR content. We first confirmed that ASGPR-targeted PFOB can be targeted specifically to hepatocytes L-02. In the healthy rat group, ASGPR-targeted PFOB increased the echo intensity (EI) of the liver by 87.47 dB, which was significantly higher than the EI increase observed with PFOB treatment (37.38 dB; P < 0.001), and the mean elimination times of the contrast agents were 282 ± 13.17 min and 225 ± 10.80 min for the ASGPR-targeted PFOB and PFOB groups, respectively (P < 0.001). In the CCl4-induced acute liver injury group, significant differences were observed in each group before and after administration of ASGPR-targeted PFOB. Significant differences were also observed between the different groups. The degree of reduction in peak EI correlated with the total dose of the CCl4. A decline in ASGPR content was correlated with the severity of acute liver damage using the CCl4-induced model. These findings suggest that ASGPR-targeted PFOB enhances ultrasound imaging and is a reliable tool for assessing the severity of acute liver damage in rats.
去唾液酸糖蛋白受体（ASGPR）是肝细胞中的一种内吞性C型凝集素受体。急慢性肝病均可导致该受体表达和含量降低。本研究的目的是确定靶向ASGPR的全氟辛基溴（PFOB）是否能增强超声成像信号，并评估四氯化碳（CCl4）诱导的大鼠急性肝损伤的严重程度。研究了靶向ASGPR的PFOB对肝细胞L-02的特异性。所有大鼠均接受靶向ASGPR的PFOB或PFOB治疗，并对肝脏进行超声成像，以评估这些治疗对成像信号的影响。还通过测量凋亡肝细胞百分比和ASGPR含量来检查CCl4注射的效果。我们首先证实靶向ASGPR的PFOB可以特异性靶向肝细胞L-02。在健康大鼠组中，靶向ASGPR的PFOB使肝脏的回声强度（EI）增加了87.47dB，显著高于PFOB治疗组观察到的EI增加（37.38dB；P<0.001），靶向ASGPR的PFOB组和PFOB组造影剂的平均消除时间分别为282±13.17分钟和225±10.80分钟（P<0.001）。在CCl4诱导的急性肝损伤组中，给药靶向ASGPR的PFOB前后各组均观察到显著差异。不同组之间也观察到显著差异。EI峰值降低程度与CCl4总剂量相关。使用CCl4诱导模型，ASGPR含量下降与急性肝损伤严重程度相关。这些发现表明，靶向ASGPR的PFOB可增强超声成像，是评估大鼠急性肝损伤严重程度的可靠工具。
