Noscapine protects the H9c2 cardiomyocytes of rats against oxygen–glucose deprivation/reperfusion injury

Vahabzadeh, Gelareh; Soltani, Hamidreza; Barati, Mahmood; Golab, Fereshteh; Jafari‐Sabet, Majid; Safari, Sepideh; Moazam, Ashrafolsadat; Mohamadrezaei, Hananeh

doi:10.1007/s11033-020-05549-6

Cited by 7 publications

(6 citation statements)

References 37 publications

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“…It suggests that noscapine is a cardiac protective agent against NO damage. The results of this study showed that BD1047 increases NO levels in H9C2 cells, and noscapine significantly inhibits NO accumulation dose-dependently (4 μ M) [ 101 ]. Noscapine exerts its protective effect on the heart by binding to and activating the sigma-1 receptors, preventing necrosis and apoptosis in cardiomyocytes [ 100 ].…”

Section: Targets Of Noscapine Receptors and Signalling Pathwaysmentioning

confidence: 99%

Noscapine, an Emerging Medication for Different Diseases: A Mechanistic Review

Rahmanian-Devin

Rahimi

Jaafari

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Noscapine is a benzylisoquinoline alkaloid isolated from poppy extract, used as an antitussive since the 1950s, and has no addictive or euphoric effects. Various studies have shown that noscapine has excellent anti-inflammatory effects and potentiates the antioxidant defences by inhibiting nitric oxide (NO) metabolites and reactive oxygen species (ROS) levels and increasing total glutathione (GSH). Furthermore, noscapine has indicated antiangiogenic and antimetastatic effects. Noscapine induces apoptosis in many cancerous cell types and provides favourable antitumour activities and inhibitory cell proliferation in solid tumours, even drug-resistant strains, via mitochondrial pathways. Moreover, this compound attenuates the dynamic properties of microtubules and arrests the cell cycle in the G2/M phase. Noscapine can reduce endothelial cell migration in the brain by inhibiting endothelial cell activator interleukin 8 (IL-8). In fact, this study aimed to elaborate on the possible mechanisms of noscapine against different disorders.

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Section: Targets Of Noscapine Receptors and Signalling Pathwaysmentioning

confidence: 99%

Noscapine, an Emerging Medication for Different Diseases: A Mechanistic Review

Rahmanian-Devin

Rahimi

Jaafari

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…After 24 h, the cells were cultured for 48 h using a medium containing 50 μM isoproterenol (ISO) to imitate the HF model (Wang et al 2021 ). Dividing the cell experiment into two parts, part one: (a) control group; (b) ISO medium group; (c) ISO medium + Ad-control group; (d) ISO medium + Ad-S1R group; (e) ISO medium + Ad-S1R + 5 μM BD1047 group (Vahabzadeh et al 2020 ). Part two: (a) control group; (b) control medium + Ad-S1R group; (c) control medium + Ad-S1R + 50 μM AG490 group (Zhao et al 2018 ); (d) ISO medium group; (e) ISO medium + Ad-S1R group (e) ISO medium + Ad-S1R + 50 μM AG490 group.…”

Section: Methodsmentioning

confidence: 99%

“…Heart failure (HF) is defined as a terminal stage of developmental cardiac disease, at which heart cannot pump adequate blood to various organs to meet the physiological demands ascribed to systolic and/or diastolic dysfunction (Meer et al 2019). Heart failure involves the activation of multiple endogenous neuroendocrine and cytokines, and the long-term activation contributes to myocardial damage and ventricular remodeling, while current therapies do not completely reverse these pathophysiological alterations (Liang et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Activation of the sigma-1 receptor exerts cardioprotection in a rodent model of chronic heart failure by stimulation of angiogenesis

Zhao

Liu

Chen

et al. 2022

Mol Med

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Background Angiogenesis plays a critical role on post-infarction heart failure (PIHF), the presence of which facilitates additional blood supply to maintain the survival of residual cardiomyocytes. The sigma-1 receptor (S1R) has been substantiated to stimulate angiogenesis, with the effect on a model of PIHF remaining unknown. Aims This study aims to investigate the effects of S1R on PIHF and the underlying mechanisms involved. Methods Rats were implemented left anterior descending artery ligation followed by rearing for 6 weeks to induce a phenotype of heart failure. Daily intraperitoneal injection of S1R agonist or antagonist for 5 weeks was applied from 2nd week after surgery. The effects exerted by S1R were detected by echocardiography, hemodynamic testing, western blot, Sirius red dyeing, ELISA, immunohistochemistry and fluorescence. We also cultured HUVECs to verify the mechanisms in vitro. Results Stimulation of S1R significantly ameliorated the cardiac function resulted from PIHF, in addition to the observation of reduced fibrosis in the peri-infarct region and the apoptosis of residual cardiomyocytes, which were associated with augmentation of microvascular density in peri-infarct region through activation of the JAK2/STAT3 pathway. We also indicated that suppression of JAK2/STAT3 pathway by specific inhibitor in vitro reversed the pro-angiogenic effects of S1R on HUVECs, which further confirmed that angiogenesis, responsible for PIHF amelioration, by S1R stimulation was in a JAK2/STAT3 pathway-dependent manner. Conclusion S1R stimulation improved PIHF-induced cardiac dysfunction and ventricular remodeling through promoting angiogenesis by activating the JAK2/STAT3 pathway.

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“…Cells were seeded at an optimized density of 5 × 10 4 cells/well in a 96-well plate, leaving 3 empty wells as controls. The MTT assay was performed as previously described [51], the cells were incubated at 37 • C for 24 h, and then treated with 100 µg/mL of DMSO-solved fractions for 2 h at a final DMSO concentration of 0.5%. After pretreatment with fractions, cells were subjected to 6-OHDA challenge at the working concentration of 60 µM in FBS-free media, followed by incubation for another 24 h. To quantify cell viability based on mitochondrial function, the cells were incubated with 0.5 mg/mL MTT and incubated for 4 h at 37 • C. To dissolve insoluble formazan crystals produced from reducing MTT by the cells, 80 µL of 20% SDS was added, and plates were wrapped with foil and placed on an orbital shaker at 100 rpm for 4 h at room temperature.…”

Section: Cell Viability Assaysmentioning

confidence: 99%

A High-Throughput Screening of a Natural Products Library for Mitochondria Modulators

Makinde,

Ma,

Mellick

et al. 2024

Biomolecules

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Mitochondria, the energy hubs of the cell, are progressively becoming attractive targets in the search for potent therapeutics against neurodegenerative diseases. The pivotal role of mitochondrial dysfunction in the pathogenesis of various diseases, including Parkinson’s disease (PD), underscores the urgency of discovering novel therapeutic strategies. Given the limitations associated with available treatments for mitochondrial dysfunction-associated diseases, the search for new potent alternatives has become imperative. In this report, we embarked on an extensive screening of 4224 fractions from 384 Australian marine organisms and plant samples to identify natural products with protective effects on mitochondria. Our initial screening using PD patient-sourced olfactory neurosphere-derived (hONS) cells with rotenone as a mitochondria stressor resulted in 108 promising fractions from 11 different biota. To further assess the potency and efficacy of these hits, the 11 biotas were subjected to a subsequent round of screening on human neuroblastoma (SH-SY5Y) cells, using 6-hydroxydopamine to induce mitochondrial stress, complemented by a mitochondrial membrane potential assay. This rigorous process yielded 35 active fractions from eight biotas. Advanced analysis using an orbit trap mass spectrophotometer facilitated the identification of the molecular constituents of the most active fraction from each of the eight biotas. This meticulous approach led to the discovery of 57 unique compounds, among which 12 were previously recognized for their mitoprotective effects. Our findings highlight the vast potential of natural products derived from Australian marine organisms and plants in the quest for innovative treatments targeting mitochondrial dysfunction in neurodegenerative diseases.

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Noscapine protects the H9c2 cardiomyocytes of rats against oxygen–glucose deprivation/reperfusion injury

Cited by 7 publications

References 37 publications

Noscapine, an Emerging Medication for Different Diseases: A Mechanistic Review

Noscapine, an Emerging Medication for Different Diseases: A Mechanistic Review

Activation of the sigma-1 receptor exerts cardioprotection in a rodent model of chronic heart failure by stimulation of angiogenesis

A High-Throughput Screening of a Natural Products Library for Mitochondria Modulators

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