Andrographolide protects against isoproterenol-induced myocardial infarction in rats through inhibition of L-type Ca2+ and increase of cardiac transient outward K+ currents

Elasoru, Seyi Elijah; Rhana, Paula; Barreto, Tatiane de Oliveira; Souza, Dayane Lorena Naves de; Menezes-Filho, José Evaldo Rodrigues de; Souza, Diego Santos; Moreira, Matheus Vilardo Lóes; Campos, Marco Túlio Gomes; Adedosu, Olaniyi T.; Roman‐Campos, Danilo; Melo, Marília Martins; Cruz, Jáder Santos

doi:10.1016/j.ejphar.2021.174194

Cited by 32 publications

(20 citation statements)

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“…Disorganized fibroblasts and some macrophages were seen in HE‐stained heart tissue sections. Similar results with these MI experimental models have been previously reported (Elasoru et al, 2021; Goyal et al, 2015; Panda, Kar, & Biswas, 2017). Treatment with Lq markedly attenuated the morphological changes of myocardial tissue with few fibroblasts and macrophages along with minimized swelling.…”

Section: Resultssupporting

confidence: 91%

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Zhang

et al. 2022

Phytotherapy Research

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Liquiritigenin (Lq) offers cytoprotective effects against various cardiac injuries, but its beneficial effects on myocardial ischemic (MI) injury and the related mechanisms remain unclear. In the in vivo study, an animal model of MI was induced by intraperitoneal injection of isoproterenol (Iso, 85 mg/kg). ECG, heart rate, serum levels of CK and CK‐MB, histopathological changes, and reactive oxygen species (ROS) levels were all measured. In vitro, H9c2 cells were divided into four groups and treated for 24 hr with liquiritigenin (30 μmol/L and 100 μmol/L) followed with CoCl2 (800 μmol/L) for another 24 hr. Cell viability, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration ([Ca2+]i) were then assessed. The L‐type Ca2+ current (ICa‐L) was detected using a patch clamp technique on isolated rat ventricular myocytes. The myocyte contraction and Ca2+ transients were measured using an IonOptix detection system. The remarkable cardiac injury and generation of intracellular ROS induced by Iso were alleviated via treatment with Lq. CoCl2 administration induced cell apoptosis, mitochondrial dysfunction, and Ca2+ overload in H9c2; Lq reduces these deleterious effects of CoCl2. Meanwhile, Lq blocked ICa‐L in a dose‐dependent manner. The half‐maximal inhibitory concentration of Lq was 110.87 μmol/L. Lq reversibly reduced the amplitude of cell contraction as well as the Ca2+ transients. The results show that Lq protects against MI injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and inhibition of ICa‐L, thus damping intracellular Ca2+.

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Section: Resultssupporting

confidence: 91%

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Zhang

et al. 2022

Phytotherapy Research

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“…The extract was injected into the stomach via the esophagus using a stainless-steel needle linked to a plastic syringe. Bodyweight, behavioral and mood changes, clinical symptoms of pain or discomfort, and animal mortality were all tracked for 28 days [ 66 ].…”

Section: Methodsmentioning

confidence: 99%

Possible Mechanisms Underlying the Antispasmodic, Bronchodilator, and Antidiarrheal Activities of Polarity–Based Extracts of Cucumis sativus L. Seeds in In Silico, In Vitro, and In Vivo Studies

et al. 2022

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Apart from the nutritional value, Cucumis sativus L. has also been used in the traditional medicine of Iran, Pakistan, and India. Its seeds are used by herbalists to treat gastrointestinal, respiratory, and urinary problems. However, more investigations are required to explain its mechanisms for treating GI, respiratory, and urinary diseases. Accordingly, the aim of the present work was to investigate the antispasmodic, bronchodilator, and antidiarrheal activities of C. sativus seeds extracts and the underlying mechanisms of action. For this purpose, sequential extracts of C. sativus seeds were prepared in n-hexane, dichloromethane, ethanol, and water. Bioactive compounds in C. sativus seed extracts were identified and quantified by utilizing LC ESI–MS/MS and HPLC. Moreover, network pharmacology and molecular docking were employed to examine the antispasmodic and bronchodilator effects of the bioactive substances in the extracts. In vitro and in vivo experiments were also conducted to validate the mechanistic insights gained from the in silico analysis. Results indicated the presence of kaempferol with a concentration of 813.74 µg/g (highest concentration) in the seed extract of C. sativus, followed by quercetin (713.83 µg/g), narcissin (681.87 µg/g), and orientin (676.19 µg/g). In silico investigations demonstrated that the bioactive chemicals in C. sativus seeds inhibited the expression of the target genes involved in smooth muscle contraction and calcium-mediated signaling. Sequential seed extracts of C. sativus caused a dose-dependent relaxant response for spasmolytic reaction and resulted in a relaxation of K+ (80 mM) spastic contraction. In animal models, C. sativus seed extracts exhibited partial or complete antiperistalsis, antidiarrheal, and antisecretory actions. By modulating the contractile response through calcium-mediated signaling target proteins, C. sativus seeds generated bronchodilator, antispasmodic, and antidiarrheal therapeutic effects.

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“…Therefore, in our research, we elucidate the ameliorating effect of 18β‐GA on myocardial infarction and its possible mechanisms. In this study, we used ISO to induce myocardial infarction; this myocardial infarction model is widely used to evaluate cardioprotective drugs (Elijah et al., 2021 ; Patel et al., 2010 ; Upaganlawar et al., 2009 ). The results indicate that 18β‐GA can protect ISO‐induced acute myocardial infarction by reducing oxidative stress, inflammation, and apoptosis through the PI3K/Akt pathway and inhibiting contractility and Ca 2+ influx via LTCC.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca²⁺ influx via L‐type Ca²⁺ channels

Chu

Wang

Zhang

et al. 2021

Food Science & Nutrition

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Andrographolide protects against isoproterenol-induced myocardial infarction in rats through inhibition of L-type Ca2+ and increase of cardiac transient outward K+ currents

Cited by 32 publications

References 50 publications

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Possible Mechanisms Underlying the Antispasmodic, Bronchodilator, and Antidiarrheal Activities of Polarity–Based Extracts of Cucumis sativus L. Seeds in In Silico, In Vitro, and In Vivo Studies

Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca²⁺ influx via L‐type Ca²⁺ channels

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Andrographolide protects against isoproterenol-induced myocardial infarction in rats through inhibition of L-type Ca2+ and increase of cardiac transient outward K+ currents

Cited by 32 publications

References 50 publications

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca2+ channels

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca2+ channels

Possible Mechanisms Underlying the Antispasmodic, Bronchodilator, and Antidiarrheal Activities of Polarity–Based Extracts of Cucumis sativus L. Seeds in In Silico, In Vitro, and In Vivo Studies

Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca2+ influx via L‐type Ca2+ channels

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Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Protective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca²⁺ influx via L‐type Ca²⁺ channels