收稿日期: 2025-04-07
网络出版日期: 2025-09-05
基金资助
国家自然科学基金资助项目(82274425)
Prevention and treatment of acute radiation⁃induced myocardial injury by the preparation of Abelmoschus manihot （L.） Medik （Jiahua Tablet）
Received date: 2025-04-07
Online published: 2025-09-05
目的 基于心肌损伤标志物以及氧化应激损伤相关指标研究黄蜀葵花制剂（甲花片）对急性放射性心肌损伤的保护效应及潜在的作用机制，为放射性心脏病的临床防治提供新策略。 方法 临床入组南京中医药大学附属医院放疗科2023年12月至2024年11月期间收治的69例胸部恶性肿瘤接受放射治疗的患者，通过随机数字表法分为对照组38例及观察组31例。对照组给予标准放射治疗联合常规放射性心肌损伤保护药物，观察组在此基础上加用甲花片，两组均连续服药1个月。于放射治疗前3 d及放射治疗后第7天比较两组患者的可溶性生长刺激表达基因2蛋白（soluble growth stimulating expression gene 2， sST2）、肌钙蛋白I（cardiac troponin I， cTnI）、超氧化物歧化酶（superoxide Dismutase， SOD）及丙二醛（malondialdehyde， MDA）水平变化。 结果 放射治疗后第7天，对照组 sST2与 cTnI 的血清浓度较干预前大幅提高（P < 0.01），观察组上述指标差异无统计学意义（P > 0.05）；组间比较，治疗后观察组sST2及cTnI水平较对照组呈现大幅下降（P < 0.05）。治疗后对照组SOD水平较治疗前大幅降低（P < 0.01）；观察组患者SOD水平较治疗前差异无统计学意义（P > 0.05）；组间比较，治疗后观察组患者SOD水平明显高于对照组（P < 0.05）。治疗后对照组MDA水平明显高于本组治疗前（P < 0.05），观察组患者MDA水平较治疗前差异无统计学意义（P > 0.05）；组间比较，治疗后观察组患者MDA水平明显低于对照组（P < 0.01）。 结论 黄蜀葵花制剂（甲花片）可有效抑制放疗诱导的急性放射性心肌损伤，其潜在的作用机制与抑制氧化应激反应有关。
杨文莉 , 包桐 , 林欣 , 牛茹歌 , 徐中驰 , 赵云贺 . 黄蜀葵花制剂防治急性放射性心肌损伤的效果[J]. 实用医学杂志, 2025 , 41(17) : 2631 -2636 . DOI: 10.3969/j.issn.1006-5725.2025.17.004
Objective To investigate the protective effects and potential mechanisms of the preparation of Abelmoschus manihot （L.） Medik （Jiahua Tablet） against acute radiation-induced myocardial injury， based on myocardial injury markers （sST2， cTnI） and oxidative stress damage-related indicators （SOD， MDA）， and to provide new avenues for the prevention and treatment of radiation-induced heart disease （RIHD）. Methods Sixty-nine patients with thoracic malignant tumor who received radiotherapy at the department of radiation oncology in Hospital Affiliated to Nanjing University of Chinese Medicine from December 2023 to November 2024 were enrolled in the study. Participants were randomly divided into control group （n = 38） and observation group （n = 31）. The control group received standard radiotherapy in conjunction with conventional medications for RIHD， while the observation group was additionally administered Jiahua Tablet alongside the same regimen. Both groups took medications continuously for 1 month. Changes in serum levels of sST2， cTnI， SOD， and MDA were compared between the two groups 3 days prior to radiotherapy and 7 days after radiological therapy. Results On day 7 post-radiotherapy， the levels of sST2 and cTnI in the control group were highly elevated， showing statistically significant difference （P < 0.01）. In contrast， the levels of sST2 and cTnI in the observation group showed only mild elevation， and no statistically significant difference was observed （P > 0.05）. Between-group analysis demonstrated that post-treatment sST2 and cTnI levels in the observation group were substantially lower compared to those in the control group， indicating statistically significant difference （P < 0.05）. After treatment， SOD level in the control group was considerably lower compared to its pre-treatment level， and marked statistical significance was observed （P < 0.01）. SOD level in the observation group demonstrated a downward trend compared to baseline value， indicating no statistical significance（P > 0.05）. Between-group analysis demonstrated that post-treatment SOD level in the observation group was substantially elevated compared to that in the control group， indicating a highly significant disparity（P < 0.05）. After treatment， MDA level in the control group was considerably higher compared to its pre-treatment level， and a marked statistical significance was observed （P < 0.05）， whereas MDA level in the observation group showed only a mild increase compared to baseline value， with no statistically significant difference （P > 0.05）.Between-group analysis demonstrated that post-treatment MDA level in the observation group was substantially lower compared to that in the control group， demonstrating a remarkably statistically significant difference （P < 0.01）. Conclusion The preparation of Abelmoschus manihot （L.） Medik （Jiahua Tablet） effectively inhibits acute radiation-induced myocardial injury， with its potential mechanism closely linked to the suppression of oxidative stress responses.
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