Alpha-lipoic acid attenuates cardiac hypertrophy via inhibition of C/EBPβ activation

Zou, Jian; Gan, Xiaohong Tracey; Zhou, Houfeng; Chen, Xiaoxiao; Guo, Yuanxin; Chen, Jia; Yang, Xiaolai; Ji, Lei

doi:10.1016/j.mce.2014.10.003

Cited by 17 publications

(13 citation statements)

References 27 publications

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“…C/EBPβ is a member of a family of basic leucine zipper transcription factors (CCAAT/enhancer-binding proteins) [19]. Previous studies demonstrated that C/EBPβ is a central indicator in both physiological and pathological hypertrophy [20, 21]. In addition, it was reported that a pivotal role of C/EBPβ in inflammation and metabolism had been identified [22].…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway

Chen¹,

Chang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Many clinical and experimental studies have shown that treatment with statins could prevent myocardial hypertrophy and remodeling induced by hypertension and myocardial infarction. But the molecular mechanism was not clear. We aimed to investigate the beneficial effects of atorvastatin on hypertension-induced myocardial hypertrophy and remodeling in spontaneously hypertensive rats (SHR) with the hope of revealing other potential mechanisms or target pathways to interpret the pleiotropic effects of atorvastatin on myocardial hypertrophy. Methods: The male and age-matched animals were randomly divided into three groups: control group (8 WKY), SHR (8 rats) and intervention group (8 SHR). The SHR in intervention group were administered by oral gavage with atorvastatin (suspension in distilled water, 10 mg/Kg once a day) for 6 weeks, and the other two groups were administered by gavage with equal quantity distilled water. Blood pressure of rats was measured every weeks using a standard tail cuff sphygmomanometer. Left ventricular (LV) dimensions were measured from short-axis views of LV under M-mode tracings using Doppler echocardiograph. Cardiomyocyte apoptosis was assessed by the TUNEL assay. The protein expression of C/EBPβ, PGC-1α and UCP3 were detected by immunohistochemistry or Western blot analysis. Results: At the age of 16 weeks, the mean arterial pressure of rats in three groups were 103.6±6.1, 151.8±12.5 and 159.1±6.2 mmHg respectively, and there wasn’t statistically significant difference between the SHR and intervention groups. Staining with Masson’s trichrome demonstrated that the increased interstitial fibrosis of LV and ventricular remodeling in the SHR group were attenuated by atorvastatin treatment. Echocardiography examination exhibited that SHR with atorvastatin treatment showed an LV wall thickness that was obviously lower than that of water-treated SHR. In hypertrophic myocardium, accompanied by increasing C/EBPβ expression and the percentage of TUNEL-positive cells, the expression of Bcl-2/Bax ratio, PGC-1α and UCP3 were reduced, all of which could be abrogated by treatment with atorvastatin for 6 weeks. Conclusion: This study further confirmed that atorvastatin could attenuate myocardial hypertrophy and remodeling in SHR by inhibiting apoptosis and reversing changes in mitochondrial metabolism. The C/EBPβ/PGC-1α/UCP3 signaling pathway might also be important for elucidating the beneficial pleiotropic effects of atorvastatin on myocardial hypertrophy.

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Section: Discussionmentioning

confidence: 99%

Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway

Chen¹,

Chang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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“…A recent study demonstrated that NFATc4 and NF- κ B could interact and assemble a transcriptional complex that effectively coordinates cardiac hypertrophy and pathological remodeling [ 35 ]. Thus, it was recently observed that the nuclear translocation of NFATc4 and the transcriptional activity of NF- κ B were significantly increased by phenylephrine, which was significantly inhibited by pretreatment with the known antioxidant alpha-lipoic acid [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Short-Term Treatment with Esmolol Reverses Left Ventricular Hypertrophy in Adult Spontaneously Hypertensive Rats via Inhibition of Akt/NF-κB and NFATc4

Quintana‐Villamandos

Goukassian

Sasi

et al. 2018

BioMed Research International

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Our group has previously demonstrated that short-term treatment with esmolol reduces left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs). The present study aimed to assess the molecular mechanisms related to this effect. Fourteen-month-old male SHRs were treated intravenously with saline as vehicle (SHR) or esmolol (SHR-E) (300 μg/kg/min). Age-matched vehicle-treated male Wistar-Kyoto (WKY) rats served as controls. After 48 hours of treatment, the hearts were harvested and left ventricular tissue was separated and processed for Western blot analysis to determine the levels of Akt, NF-κB, NFATc4, Creb1, Serca2a, Erk1/2, and Sapk/Jnk. Biomarkers of oxidative stress, such as catalase, protein carbonyls, total thiols, and total antioxidant capacity were evaluated. Esmolol reversed the levels of p-NFATc4, p-Akt, and p-NF-κB in SHRs to the phospholevels of these proteins in WKY rats without modifying p-Erk1/2, p-Sapk/Jnk, p-Creb1, or Serca2a in SHR. Compared with SHR, esmolol increased catalase activity and reduced protein carbonyls without modifying total thiols or total antioxidant capacity. Short-term treatment with esmolol reverses LVH in aged SHRs by downregulation of Akt/NF-κB and NFATc4 activity. Esmolol treatment also increases catalase activity and reduces oxidative stress in SHRs with LVH.

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“…Thioctic acid has the ability to decrease serum BNP and cardiac hypertrophy by attenuation of mRNA and protein levels of C/ EBPβ which is responsible for cardiomyocyte hypertrophy. Also, thioctic acid decrease BNP serum levels through acting directly on scavenging free radicals, increasing the activity of natural antioxidant, reduction of oxidative stress and inflammation [25]. Moreover, thioctic acid decreases the level of caspase-3 due to antioxidant, anti-inflammatory and anti-apoptotic properties against doxorubicin toxicity in rats [26].…”

Section: Apoptosismentioning

confidence: 99%

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2018

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Alpha-lipoic acid attenuates cardiac hypertrophy via inhibition of C/EBPβ activation

Cited by 17 publications

References 27 publications

Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway

Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway

Short-Term Treatment with Esmolol Reverses Left Ventricular Hypertrophy in Adult Spontaneously Hypertensive Rats via Inhibition of Akt/NF-κB and NFATc4

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