Carvedilol improves ethanol‐induced liver injury via modifying the interaction between oxidative stress and sympathetic hyperactivity in rats

Hakucho, Ayako; Liu, Jinyao; Liu, Xu; Fujimiya, Tatsuya

doi:10.1111/hepr.12143

Cited by 16 publications

(9 citation statements)

References 45 publications

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“…In accordance, our findings suggest that familial DCM hiPSC‐CMs have increased susceptibility to apoptosis and cell death after exposure to external chronotropic stress, and that pharmacological pretreatment with carvedilol or verapamil modestly reduced chronotropic stress‐induced apoptosis and cell death rate in familial DCM hiPSC‐CMs. In addition to negating inotropic and chronotropic actions, carvedilol also participates in antioxidant responses by mediating oxidative stress . Supplementary studies of the role of oxidative stress and carvedilol in RBM20 hiPSC‐CMs could be informative in modifying apoptotic response and disease progression.…”

Section: Discussionmentioning

confidence: 99%

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Pharmacological Modulation of Calcium Homeostasis in Familial Dilated Cardiomyopathy: An In Vitro Analysis From an RBM20 Patient‐Derived iPSC Model

Wyles

Hrstka

Reyes

et al. 2016

Clinical Translational Sci

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For inherited cardiomyopathies, abnormal sensitivity to intracellular calcium (Ca2+), incurred from genetic mutations, initiates subsequent molecular events leading to pathological remodeling. Here we characterized the effect of β-adrenergic stress in familial dilated cardiomyopathy (DCM) using human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs) from a patient with RBM20 DCM. Our findings suggest that β-adrenergic stimulation accelerated defective Ca2+ homeostasis, apoptotic changes and sarcomeric disarray in familial DCM hiPSC-CMs. Furthermore, pharmacological modulation of abnormal Ca2+ handling by pre-treatment with β-blocker, carvedilol, or Ca2+-channel blocker, verapamil, significantly decreased the area under curve, reduced percentage of disorganized cells, and decreased TUNEL positive apoptotic loci in familial DCM hiPSC-CMs following β-adrenergic stimulation. These translational data provide patient-based in vitro analysis of β-adrenergic stress in RBM20–deficient familial DCM hiPSC-CMs and evaluation of therapeutic interventions to modify heart disease progression, which may be personalized but more importantly generalized in the clinic.

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Section: Discussionmentioning

confidence: 99%

“…In addition to negating inotropic and chronotropic actions, carvedilol also participates in antioxidant responses by mediating oxidative stress. 45,46 Supplementary studies of the role of oxidative stress and carvedilol in RBM20 hiPSC-CMs could be informative in modifying apoptotic response and disease progression.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Modulation of Calcium Homeostasis in Familial Dilated Cardiomyopathy: An In Vitro Analysis From an RBM20 Patient‐Derived iPSC Model

Wyles

Hrstka

Reyes

et al. 2016

Clinical Translational Sci

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“…Carvedilol has been reported to be effective in various ROS-related tissue injury models (Huang et al, 2007;Rodrigues et al, 2011;Saeidnia & Abdollahi;Singh et al, 2004) such as alcoholic fatty liver disease, hepatic IR, insulin sensitivity, and sympathetic hyperactivity in rats, which can be of great interest as there is a close association between PCOS and above-mentioned disorders (Bhatt et al, 2007;Hakucho et al, 2014;Kveiborg et al, 2006). Supporting our results, administration of carvedilol also had a beneficial effect on the bone quality in ovariectomized postmenopausal rat model via estradiol enhancement, antioxidants promotion, and diminishing in resorbing TNF-a and IL-6 (Boshra & El Wakeel, 2013).…”

Section: Discussionmentioning

confidence: 99%

Dual targeting of TNF-αand free radical toxic stress as a promising strategy to manage experimental polycystic ovary

Rezvanfar

Saeedi

Mansoori

et al. 2015

Pharmaceutical Biology

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Submit your article to this journal Results: PCO rats exhibited ovarian cystogenesis which was preserved by the application of carvedilol and ANGIPARSä. In comparison with controls, decreased level of the total antioxidant power (TAP) and higher levels of reactive oxygen species (ROS) and lipid peroxidation (LPO) in serum and ovaries (2.41 ± 0.67 versus 0.72 ± 0.11; and 0.17 ± 0.04 versus 0.05 ± 0.01; 5.48 ± 1.30 versus 10.56 ± 0.77; and 7.06 ± 1.94 versus 17.98 ± 0.98; p50.05, respectively) were detected in PCO rats. Moreover, the PCO rats exhibited hyperandrogenism due to a 3.7-fold increase in serum testosterone concentration (35.04 ± 3.17 versus 131.09 ± 13.24; p50.05) along with a 2.98-fold decrease in serum progesterone (6.19 ± 0.40 versus 18.50 ± 1.03; p50.05) and 5.2-fold decrease in serum estradiol (9.30 ± 0.61 versus 48.3 ± 2.10; p50.05) when compared with those of the control group. However, similar to the control group, normal levels of OS markers and sex hormones were detected in ANGIPARSä and carvedilol co-treated PCO rats. Besides, when compared with controls, increased levels of TNF-a (770.75 ± 42.06 versus 477.14 ± 28.77; p50.05) and insulin (1.27 ± 0.10 versus 0.36 ± 0.05; p50.05) in PCO rats were significantly inhibited by carvedilol and ANGIPARSä co-treatment. Discussion and conclusion: We evidenced the beneficial effects of carvedilol and ANGIPARSä in PCO, which underpin the new alternative approach in using these kinds of medicines in female reproductive disorders.

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“…Carvedilol, another non-selective β-receptor antagonist, has been used in an animal model of alcoholic fatty liver disease and was found to attenuate oxidative stresses caused by the hypermetabolic state [140]. Given that non-selective beta-blockade appears to affect ER stress in both burn and alcohol exposures, administration in the setting of combined injury should also help prevent associated oxidative damage and the development of steatosis.…”

Section: Clinical Managementmentioning

confidence: 99%

Alcohol Modulation of the Postburn Hepatic Response

Chen

Carter

Curtis

et al. 2017

Journal of Burn Care & Research

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The widespread and rapidly increasing trend of binge drinking is accompanied by a concomitant rise in the prevalence of trauma patients under the influence of alcohol at the time of their injury. Epidemiologic evidence suggests up to half of all adult burn patients are intoxicated at the time of admission and the presence of alcohol is an independent risk factor for death in the early stages post burn. As the major site of alcohol metabolism and toxicity, the liver is a critical determinant of post burn outcome and experimental evidence implies an injury threshold exists beyond which burn-induced hepatic derangement is observed. Alcohol may lower this threshold for post burn hepatic damage through a variety of mechanisms including modulation of extrahepatic events, alteration of the gut-liver axis, and changes in signaling pathways. The direct and indirect effects of alcohol may prime the liver for the second-hit of many overlapping physiologic responses to burn injury. In an effort to gain a deeper understanding of how alcohol potentiates post burn hepatic damage, we summarize possible mechanisms by which alcohol modulates the post burn hepatic response.

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Carvedilol improves ethanol‐induced liver injury via modifying the interaction between oxidative stress and sympathetic hyperactivity in rats

Cited by 16 publications

References 45 publications

Pharmacological Modulation of Calcium Homeostasis in Familial Dilated Cardiomyopathy: An In Vitro Analysis From an RBM20 Patient‐Derived iPSC Model

Pharmacological Modulation of Calcium Homeostasis in Familial Dilated Cardiomyopathy: An In Vitro Analysis From an RBM20 Patient‐Derived iPSC Model

Dual targeting of TNF-αand free radical toxic stress as a promising strategy to manage experimental polycystic ovary

Alcohol Modulation of the Postburn Hepatic Response

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