The protective effect of zinc, selenium, and chromium on myocardial fibrosis in the offspring of rats with gestational diabetes mellitus

Deng, Haichao; Yao, Xueqiong; Cui, Ningning; Huang, Shanshan; Ge, Yanyan; Li, Rui; Yang, Xuefeng

doi:10.1039/d2fo01105k

Cited by 7 publications

(4 citation statements)

References 49 publications

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“…Previous studies have established that cathodal tDCS modified cortical metabolites such as glutamate in healthy mice (Peruzzotti‐Jametti et al., 2013). As an essential trace element, Se is associated with various metabolic pathways (Deng et al., 2023; Zhang, Chen et al., 2021). Se regulated brain glutamate and aspartate metabolism to suppress neurotoxicity (Parra‐Martínez et al., 2022).…”

Section: Discussionmentioning

confidence: 99%

Cathodal bilateral transcranial direct‐current stimulation regulates selenium to confer neuroprotection after rat cerebral ischaemia–reperfusion injury

Wang,

Ma,

et al. 2024

The Journal of Physiology

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Non‐invasive transcranial direct‐current stimulation (tDCS) is a safe ischaemic stroke therapy. Cathodal bilateral tDCS (BtDCS) is a modified tDCS approach established by us recently. Because selenium (Se) plays a crucial role in cerebral ischaemic injury, we investigated whether cathodal BtDCS conferred neuroprotection via regulating Se‐dependent signalling in rat cerebral ischaemia–reperfusion (I/R) injury. We first showed that the levels of Se and its transport protein selenoprotein P (SEPP1) were reduced in the rat cortical penumbra following I/R, whereas cathodal BtDCS prevented the reduction of Se and SEPP1. Interestingly, direct‐current stimulation (DCS) increased SEPP1 level in cultured astrocytes subjected to oxygen‐glucose deprivation reoxygenation (OGD/R) but had no effect on SEPP1 level in OGD/R‐insulted neurons, indicating that DCS may increase Se in ischaemic neurons by enhancing the synthesis and secretion of SEPP1 in astrocytes. We then revealed that DCS reduced the number of injured mitochondria in OGD/R‐insulted neurons cocultured with astrocytes. DCS and BtDCS prevented the reduction of the mitochondrial quality‐control signalling, vesicle‐associated membrane protein 2 (VAMP2) and syntaxin‐4 (STX4), in OGD/R‐insulted neurons cocultured with astrocytes and the ischaemic brain respectively. Under the same experimental conditions, downregulation of SEPP1 blocked DCS‐ and BtDCS‐induced upregulation of VAMP2 and STX4. Finally, we demonstrated that cathodal BtDCS increased Se to reduce infract volume following I/R. Together, the present study uncovered a molecular mechanism by which cathodal BtDCS confers neuroprotection through increasing SEPP1 in astrocytes and subsequent upregulation of SEPP1/VAMP2/STX4 signalling in ischaemic neurons after rat cerebral I/R injury. imageKey points Cathodal bilateral transcranial direct‐current stimulation (BtDCS) prevents the reduction of selenium (Se) and selenoprotein P in the ischaemic penumbra. Se plays a crucial role in cerebral ischaemia injury. Direct‐current stimulation reduces mitochondria injury and blocks the reduction of vesicle‐associated membrane protein 2 (VAMP2) and syntaxin‐4 (STX4) in oxygen‐glucose deprivation reoxygenation‐insulted neurons following coculturing with astrocytes. Cathodal BtDCS regulates Se/VAMP2/STX4 signalling to confer neuroprotection after ischaemia.

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Section: Discussionmentioning

confidence: 99%

Cathodal bilateral transcranial direct‐current stimulation regulates selenium to confer neuroprotection after rat cerebral ischaemia–reperfusion injury

Wang,

Ma,

et al. 2024

The Journal of Physiology

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“…However, owing to time limitations, comprehensive investigations of the impact of Sal B on the ubiquitination of Smad7 were not conducted. We speculate that Sal B may decrease the ubiquitination of Smad7 by suppressing the expression and activity of key enzymes involved in Smad7 ubiquitination, such as Smurf1 and Smurf2 [ 41 , 42 ]. Alternatively, Sal B may enhance the deubiquitination of Smad7 by increasing the expression and activity of deubiquitination enzymes such as USP2 and OTUD1 [ 43 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7

Luo,

Fu,

Wang

et al. 2023

Chin Med

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Background Salvianolic acid B (Sal B), a water-soluble phenolic compound derived from Salvia miltiorrhiza Bunge, is commonly used in Traditional Chinese Medicine to treat cardiovascular disease. In our previous study, Sal B protected against myocardial fibrosis induced by diabetic cardiomyopathy (DCM). This study aimed to investigate the ameliorative effects and potential mechanisms of Sal B in mitigating myocardial fibrosis induced by DCM. Methods Various methods were used to investigate the effects of Sal B on myocardial fibrosis induced by DCM in vivo and in vitro. These methods included blood glucose measurement, echocardiography, HE staining, Masson’s trichrome staining, Sirius red staining, cell proliferation assessment, determination of hydroxyproline levels, immunohistochemical staining, evaluation of fibrosis-related protein expression (Collagen-I, Collagen-III, TGF-β1, p-Smad3, Smad3, Smad7, and α-smooth muscle actin), analysis of Smad7 gene expression, and analysis of Smad7 ubiquitin modification. Results The animal test results indicated that Sal B significantly improved cardiac function, inhibited collagen deposition and phenotypic transformation, and ameliorated myocardial fibrosis in DCM by upregulating Smad7, thereby inhibiting the TGF-β1 signaling pathway. In addition, cell experiments demonstrated that Sal B significantly inhibited the proliferation, migration, phenotypic transformation, and collagen secretion of cardiac fibroblasts (CFs) induced by high glucose (HG). Sal B significantly decreased the ubiquitination of Smad7 and stabilized the protein expression of Smad7, thereby increasing the protein expression of Smad7 in CFs and inhibiting the TGF-β1 signaling pathway, which may be the potential mechanism by which Sal B mitigates myocardial fibrosis induced by DCM. Conclusion This study revealed that Sal B can improve myocardial fibrosis in DCM by deubiquitinating Smad7, stabilizing the protein expression of Smad7, and blocking the TGF-β1 signaling pathway.

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“…Myocardial cell viability decreased under H/R, whereas 12 h-33.3 µmol/L of G-Rg5 intervention signi cantly increased cell viability and reduced LDH levels. LDH is a living intracytoplasmic enzyme released from the cytoplasm into the external environment when cells are injured as an indicator of the degree of cell damage [58] and can indirectly re ect cell viability [59]. This suggests that G-Rg5 can reduce H/R-induced H9c2 cardiomyocyte injury.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Ginsenoside Rg5 on Hypoxia/Reoxygenation- Induced H9c2 Cardiomyocytes by Correcting Free Fatty Acids β- oxidation

Jiang

Fang

Zhang

et al. 2023

Preprint

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Clinically, the in-hospital mortality rate of cardiogenic shock (CS) is approximately 50%. In CS, metabolic pathways in the body undergo “embryonal transformation,” in which metabolic processes transform free fatty acids (FFAs) to glucose. Shenfu injection (SFI) treatment has exhibited a positive effect on cardiogenic shock, and ginsenoside Rg5 (G-Rg5) is the anticardiogenic shock component of SFI. In this study, we aimed to investigate the myocardial protective effect and mechanism of G-Rg5 in myocardial energy metabolism, especially from the perspective of FFA β-oxidation, one of the most crucial lipid metabolism pathways. Cardiomyocytes were exposed to hypoxia-reoxygenation (H/R) and treated with G-Rg5. MTT analysis was used to determine the viability of H9c2 cardiomyocytes under different interventions with G-Rg5. The levels of lactate dehydrogenase (LDH) and FFA were detected using ELISA, and adenosine triphosphate (ATP) was determined using high-performance liquid chromatography (HPLC). Furthermore, the expression of NR4A1 was determined by RT-qPCR, and the levels of AMPKα, p-AMPKα, and GPX4 were detected by western blotting to explore the underlying mechanism. We observed that G-Rg5-protected H9c2 cardiomyocytes exhibited better FFA β-oxidation regulation, thereby producing an increased abundance of ATP. G-Rg5 may correct FFA β-oxidation by regulating the levels of NR4A1, AMPKα, p-AMPKα, and GPX4. Therefore, G-Rg5 is a promising drug for CS treatment.

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The protective effect of zinc, selenium, and chromium on myocardial fibrosis in the offspring of rats with gestational diabetes mellitus

Abstract: Myocardial fibrosis in offspring with hyperglycemia is confirmed first; supplementation with zinc, selenium, and chromium to GDM mothers suppresses these changes in offspring.

Cited by 7 publications

References 49 publications

Cathodal bilateral transcranial direct‐current stimulation regulates selenium to confer neuroprotection after rat cerebral ischaemia–reperfusion injury

Cathodal bilateral transcranial direct‐current stimulation regulates selenium to confer neuroprotection after rat cerebral ischaemia–reperfusion injury

Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7

Protective Effect of Ginsenoside Rg5 on Hypoxia/Reoxygenation- Induced H9c2 Cardiomyocytes by Correcting Free Fatty Acids β- oxidation

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