Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein |
| |
| Authors: | Zhantu Liu Lili Yang Jiyi Huang Ping Xu Zeyu Zhang Dong Yin Jichun Liu Huan He Ming He |
| |
| Affiliation: | 1. Jiangxi Provincial Institute of Hypertension, the First Affiliated Hospital, Nanchang University, Nanchang, China;2. Department of Pharmacy, Nanchang School of Hygiene, Nanchang, China;3. Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University School of Pharmaceutical Science, Nanchang, China;4. Jiangxi Provincial Key Laboratory of Molecular Medicine, the Second Affiliated Hospital, Nanchang University, Nanchang, China |
| |
| Abstract: | ![]()
Ischemia/reperfusion (I/R) injury is the major cause of acute cardiovascular disease worldwide. 14‐3‐3η protein has been demonstrated to protect myocardium against I/R injury. Luteoloside (Lut), a flavonoid found in many Chinese herbs, exerts myocardial protection effects. However, the mechanism remains unclear. We hypothesize that the cardioprotective role of Lut is exerted by regulating the 14‐3‐3η signal pathway. To investigate our hypothesis, an in vitro I/R model was generated in H9C2 cardiomyocytes by anoxia/reoxygenation (A/R) treatment. The effects of Lut on cardiomyocytes with A/R injury were assessed by determining the cell viability, lactate dehydrogenase levels, intracellular reactive oxygen species levels, mitochondrial permeability transition pores (mPTP) openness, caspase‐3 activity, and apoptosis rate. The effects on protein expression were tested using western blot analysis. Lut attenuated A/R‐induced injury to cardiomyocytes by increasing the expression of 14‐3‐3η protein and cell viability; decreasing levels of lactate dehydrogenase, reactive oxygen species, mPTP openness, caspase‐3 activity, and low apoptosis rate were observed. However, the cardioprotective effects of Lut were blocked by AD14‐3‐3ηRNAi, an adenovirus knocking down the intracellular 14‐3‐3η expression. In conclusion, to our knowledge, this is the first study to demonstrate that Lut protected cardiomyocytes from A/R‐induced injury via the regulation of 14‐3‐3η signaling pathway. |
| |
| Keywords: | 14‐3‐3η anoxia/reoxygenation cardioprotection Luteoloside mitochondria‐dependent apoptosis |
|
|
