Curcumin Ameliorates Cisplatin-Induced Cardiovascular Injuries by Upregulating ERK/p-ERK Expression in Rats.
10.1007/s11655-025-4017-4
- Author:
Jun-Tao HAO
1
;
Meng-Piao LIN
2
;
Jin WANG
2
;
Feng SONG
3
;
Xiao-Jie BAI
4
,
5
Author Information
1. Department of Thoracic Surgery, the Fifth Hospital of Shanxi Medical University, Taiyuan, 030012, China.
2. Department of Physiology, and Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, 030001, China.
3. Basic Medical College, Shanxi Medical University, Jinzhong, Shanxi Province, 030600, China.
4. Department of Physiology, and Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, 030001, China. baixiaojie_1973@
5. com.
- Publication Type:Journal Article
- Keywords:
cardiovascular toxicity;
cisplatin;
curcumin;
extracellular signal-regulated kinase
- MeSH:
Animals;
Curcumin/therapeutic use*;
Cisplatin/adverse effects*;
Rats, Sprague-Dawley;
Male;
Up-Regulation/drug effects*;
Extracellular Signal-Regulated MAP Kinases/metabolism*;
Phosphorylation/drug effects*;
Electrocardiography;
Blood Pressure/drug effects*;
Rats;
MAP Kinase Signaling System/drug effects*
- From:
Chinese journal of integrative medicine
2025;31(8):717-725
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate cisplatin-induced cardiovascular toxicity and explore the protective effects and potential mechanism of curcumin co-treatment.
METHODS:Forty adult male Sprague-Dawley rats were numbered and randomly divided into control group, cisplatin group (7.5 mg/kg, once a week, for 2 weeks), curcumin group (200 mg/kg per day, for 2 weeks) and cisplatin+curcumin group (cisplatin 7.5 mg/kg, once a week, and curcumin 200 mg/kg per day for 2 weeks) by a random number table method, with 10 rats in each group. Cardiac and vascular morphology and functions were assessed using hematoxylin-eosin and Masson's trichrome staining, serum indexes detection, echocardiography, electrocardiogram (ECG), blood pressure monitoring, vascular ring isometric tension measurement, and left ventricular pressure evaluation. The expressions of extracellular signal-regulated kinases (ERK) and phosphorylated-ERK (p-ERK) were analyzed by immunohistochemical staining.
RESULTS:Cisplatin treatment induced notable cardiac alteration, as evidenced by changes in cardiac morphology, elevated serum enzymes (P<0.05), ECG abnormalities, and increased left ventricular end-diastolic pressure (P<0.05). Meanwhile, cisplatin significantly increased arterial pulse pressure (P<0.01), primarily due to a decrease in diastolic blood pressure. Severe fibrosis was also observed in the thoracic aorta wall. In vascular ring experiments, cisplatin treatment led to a significant reduction in phenylephrine-induced contraction (P<0.05) and acetylcholine-induced relaxation (P<0.01). Notably, Curcumin co-administration significantly alleviated cisplatin-induced cardiovascular damages, as demonstrated by improvement in these parameters. Furthermore, ERK expression in the myocardium and p-ERK expression in vascular smooth muscle cells were significantly upregulated following curcumin co-treatment.
CONCLUSIONS:Curcumin protects the heart and vasculature from cisplatin-induced damages, likely by upregulating ERK/p-ERK expression. These findings suggest that curcumin may serve as a promising therapeutic strategy for mitigating cisplatin-associated cardiovascular toxicity during tumor chemotherapy. In vitro cell culture experiments are needed to clarify the underlying mechanism.
