Cell therapy in dilated cardiomyopathy: from animal models to clinical trials

Carvalho, Antônio Carlos Campos de

doi:10.1590/s0100-879x2011007500047

Cited by 4 publications

(4 citation statements)

References 30 publications

(30 reference statements)

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“…Moreover, inflammation and apoptosis of cardiomyocytes are also prominent pathological features in other cardiovascular diseases such as sepsis, nerve damage, and myocardial infarction injury 3–6 . While traditional therapies to prevent cardiomyocyte inflammation and apoptosis remain ineffective, research has focused on new strategies 7–11 …”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5][6] While traditional therapies to prevent cardiomyocyte inflammation and apoptosis remain ineffective, research has focused on new strategies. [7][8][9][10][11] Lipopolysaccharide (LPS) is involved in regulating the initiation of pathophysiological cascades. 12 Previous literature reported that reduction of LPS could improve outcomes in patients with cardiac disease.…”

Section: Introductionmentioning

confidence: 99%

“… 3 , 4 , 5 , 6 While traditional therapies to prevent cardiomyocyte inflammation and apoptosis remain ineffective, research has focused on new strategies. 7 , 8 , 9 , 10 , 11 …”

Section: Introductionmentioning

confidence: 99%

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Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway

Xie,

Yang,

2023

Immunity Inflam & Disease

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IntroductionHesperetin (HES), whose main pharmacological effects are anti‑inflammatory and cardioprotective properties. In our study, we investigated the role of HES in lipopolysaccharide (LPS)‐induced inflammation and apoptosis in H9c2 cells.MethodsCell viability was assessed through MTT assay. Tumor necrosis factor (TNF)‐α and interleukin (IL)‐β expression were quantified through RT‐qPCR assay. Secondly, the apoptosis rate was assessed by Terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling assay. Finally, B‐cell lymphoma 2 (Bcl‐2)‐ associated X protein (Bax), adenosine monophosphate‐activated protein kinase (AMPK), and P53 expression were quantified through western blot assay.ResultsOur results demonstrated that LPS stimulation decreased the cell viability, increased IL‐1β and TNF‐α expression in H9c2 cells. However, HES treatment significantly increased the cell viability, decreased IL‐1β and TNF‐α expression in LPS‐induced H9c2 cells. In addition, HES significantly increased the phosphorylation level of AMPK. Meanwhile, HES prevented against LPS‐mediated the P53 and Bax protein upregulation, and Bcl‐2 protein downregulation in H9c2 cells. More interestingly, compound C (an AMPK inhibitor) treatment eliminated the protective effects of HES.ConclusionOur findings revealed that HES attenuated the LPS‐mediated inflammation and apoptosis of H9c2 cells by activating the AMPK/P53 signaling pathway, suggesting that HES may be a potential cardioprotective agent.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway

Xie,

Yang,

2023

Immunity Inflam & Disease

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“…Inflammation and apoptosis of cardiomyocytes is a key feature of a variety of pathological conditions in various cardiovascular diseases, including sepsis, ischemia/reperfusion injury, myocardial infarction and end-stage heart failure (3)(4)(5)(6). The traditional therapies preventing inflammatory responses and apoptosis of cardiomyocytes remain ineffective, so studies have focused on novel strategies (7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Hesperetin attenuates mitochondria-dependent apoptosis in lipopolysaccharide-induced H9C2 cardiomyocytes

Zheng

Liu

Deng

et al. 2014

Molecular Medicine Reports

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Apoptosis is closely associated with the occurrence and development of cardiovascular diseases and is considered as one of the crucial pathological processes of cardiomyopathy, sepsis, ischemia/reperfusion injury, myocardial infarction and heart failure. Hesperetin (HES), a flavanone glycoside found in citrus fruit peels, has been known to exhibit several key biological and pharmacological properties. Previous studies have demonstrated the anti-inflammatory, anti-oxidant and anti-tumor functions of HES. However, with regards to the pro- or anti-apoptotic functions of HES, there are several disagreements within the literature. To examine whether HES has protective effects in cardiac apoptosis, the present study examined the role of HES in lipopolysaccharide (LPS)-stimulated H9C2 cardiomyocytes, aiming to clarify the possible mechanisms underlying its effects. In the present study, HES reduced the percentage of viable apoptotic (VA) cells in a flow cytometry analysis. It had an anti-apoptosis function in LPS-stimulated H9C2 cells. To clarify whether HES alleviated LPS-stimulated apoptosis through the mitochondria-dependent intrinsic apoptotic pathway, certain indicators of this pathway were detected, including members of the caspase family. The data revealed that HES attenuated the activation of capase-3 and caspase-9. These results indicated HES has a mitochondria-dependent anti-apoptosis effect in LPS-stimulated H9C2 cells. To explore the possible mechanisms, the protein expression levels of certain markers in the possible signaling pathway were detected, including JNK and Bcl-2 family. As a result, HES downregulated the protein expression of Bax, upregulated the expression of Bcl-2 and attenuated the phosphorylation level of JNK. Therefore, the anti-apoptosis effects of HES were possibly mediated by the JNK/Bax signaling pathway. In conclusion, HES has a mitochondria-dependent anti-apoptosis effect in LPS-induced H9C2 cells via the JNK/Bax signaling pathway.

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