Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways

Abstract

BackgroundLysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes.MethodsCell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay.ResultsWe found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase-9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC-induced ERK1/2, JNK, and p38 activations were inhibited by baicalein.ConclusionsBaicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways.

Anti-inflammatory and anti-apoptotic effects of the combination of Ligusticum chuanxiong and Radix Paeoniae against focal cerebral ischaemia via TLR4/MyD88/MAPK/NF-κB signalling pathway in MCAO rats

“…p38 MAPK is reported to be activated by ischaemia, and downregulation of p38MAPK could reduce the brain injury and neurological deficits in cerebral focal ischaemia . The decreased p‐p38 and elevated p‐ERK1/2 contribute to neuro‐protection in ischaemia stroke . Based on these, we explored the potential mechanisms of anti‐inflammatory effect after ischaemic injury.…”

“…[44] The decreased p-p38 and elevated p-ERK1/2 contribute to neuro-protection in ischaemia stroke. [45] Based on these, we explored the potential mechanisms of anti-inflammatory effect after ischaemic injury. CX, CS and XS treatment significantly decreased the higher expression of TLR4, TLR5, NF-jB and p-p38MAPK induced by stroke and increased the p-ERK expressions.…”

Geniposide Prevents Hypoxia/Reoxygenation-Induced Apoptosis in H9c2 Cells: Improvement of Mitochondrial Dysfunction and Activation of GLP-1R and the PI3K/AKT Signaling Pathway

“…Physiological levels of ROS/RNS in normal oxidative metabolism play a key homeostatic role in balancing disposal rates of oxidative pressure and enzyme systems in cell proliferation and survival [27][28][29]. As levels of SOD, glutathione, and catalase are less in the cardiac system, excessive production of ROS/RNS triggers oxidative stress and aggravates ischemia-induced cardiomyocyte damage [27,30], further accelerating cardiomyocyte apoptosis and loss [31,32]. Treatment with antioxidant agents or upregulation of endogenous antioxidant enzymes could prevent excessive ROS-caused injury [4,33,34].…”

MicroRNA-18a enhances the radiosensitivity of cervical cancer cells by promoting radiation-induced apoptosis

“…The nuclear morphology of the cells was visualized using an inverted fluorescence microscope. The cells showing nuclear fragmentation and chromatin condensation in Hoechst staining were considered apoptotic cells (10). Three independent experiments were performed in triplicate.…”