Mangiferin protect myocardial insults through modulation of MAPK/TGF-β pathways

Suchal, Kapil; Malik, Salma; Gamad, Nanda; Malhotra, Rajiv; Goyal, Sameer N.; Ojha, Shreesh; Kumari, Santosh; Bhatia, Jagriti; Arya, Dharamvir Singh

doi:10.1016/j.ejphar.2016.02.055

Cited by 48 publications

(33 citation statements)

References 31 publications

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“…The myocardial IR injury was performed according to the previous procedure (Suchal et al ., ref. 23 ). Briefly, diabetic rats were anaesthetized with pentobarbitone sodium.…”

Section: Methodsmentioning

confidence: 99%

Protective effect of mangiferin on myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats: role of AGE-RAGE/MAPK pathways

Suchal

Malik

Khan

et al. 2017

Sci Rep

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Hyperglycemia induced advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) activation is thought to involve in the development of cardiovascular disease in diabetics. Activation of AGE-RAGE axis results in the oxidative stress and inflammation. Mangiferin is found in the bark of mango tree and is known to treat diseases owing to its various biological activities. Thus, this study was designed to evaluate the effect of mangiferin in ischemia-reperfusion (IR) induced myocardial injury in diabetic rats. A single injection of STZ (70 mg/kg; i.p.) was injected to male albino Wistar rats to induce diabetes. After confirmation of diabetes, rats were administered vehicle (2 ml/kg; i.p.) and mangiferin (40 mg/kg; i.p.) for 28 days. On 28th day, left anterior descending coronary artery was ligated for 45 min and then reperfused for 60 min. Mangiferin treatment significantly improved cardiac function, restored antioxidant status, reduced inflammation, apoptosis and maintained myocardial architecture. Furthermore, mangiferin significantly inhibited the activation of AGE-RAGE axis, c-Jun N-terminal kinase (JNK) and p38 and increased the expression of extracellular regulated kinase 1/2 (ERK1/2) in the myocardium. Thus, mangiferin attenuated IR injury in diabetic rats by modulation of AGE-RAGE/MAPK pathways which further prevented oxidative stress, inflammation and apoptosis in the myocardium.

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“…The myocardial IR injury was performed according to the previous procedure (Suchal et al ., ref. 23 ). Briefly, diabetic rats were anaesthetized with pentobarbitone sodium.…”

Section: Methodsmentioning

confidence: 99%

Protective effect of mangiferin on myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats: role of AGE-RAGE/MAPK pathways

Suchal

Malik

Khan

et al. 2017

Sci Rep

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“…A regulatory role of MG on MAPK and monocyte chemoattractant protein-1, which attracts monocytes and memory T lymphocytes, has been reported (Leiro et al, 2004;Suchal et al, 2016;Tsubaki et al, 2015). Particularly, the genes coding the JNK1/2 MAPKs, which are key roles in the induction of COX-2 gene expression in macrophages are inhibited by MG (Leiro et al, 2004).…”

Section: Mg Inhibits the Corresponding Gene Expression And Protein Symentioning

confidence: 93%

“…Pharmacological inhibition of IL‐1β, JNK, monocyte chemoattractant protein‐1, or MMP‐2 signaling via spinal administration has been shown to attenuate inflammatory and neuropathic pain (Watkins et al, ). A regulatory role of MG on MAPK and monocyte chemoattractant protein‐1, which attracts monocytes and memory T lymphocytes, has been reported (Leiro et al, ; Suchal et al, ; Tsubaki et al, ). Particularly, the genes coding the JNK1/2 MAPKs, which are key roles in the induction of COX‐2 gene expression in macrophages are inhibited by MG (Leiro et al, ).…”

Section: Introducing Mangiferin In the Mixed Oa Pain Treatmentmentioning

confidence: 97%

Mangiferin: Possible uses in the prevention and treatment of mixed osteoarthritic pain

Garrido-Suárez

Garrido

Piñeros

et al. 2019

Phytotherapy Research

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Osteoarthritis (OA) pain has been proposed to be a mixed pain state, because in some patients, central nervous system factors are superimposed upon the more traditional peripheral factors. In addition, a considerable amount of preclinical and clinical evidence has shown that, accompanying the central neuroplasticity changes and partially driven by a peripheral nociceptive input, a real neuropathic component occurs that are particularly linked to disease severity and progression. Hence, innovative strategies targeting neuroprotection and particularly neuroinflammation to prevent and treat OA pain could be introduced. Mangiferin (MG) is a glucosylxanthone that is broadly distributed in higher plants, such as Mangifera indica L. Previous studies have documented its analgesic, anti‐inflammatory, antioxidant, neuroprotective, and immunomodulatory properties. In this paper, we propose its potential utility as a multitargeted compound for mixed OA pain, even in the context of multimodal pharmacotherapy. This hypothesis is supported by three main aspects: the cumulus of preclinical evidence around this xanthone, some preliminary clinical results using formulations containing MG in clinical musculoskeletal or neuropathic pain, and by speculations regarding its possible mechanism of action according to recent advances in OA pain knowledge.

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“…TNF‐α, a multifunctional cytokine, has been reported to activate inflammation via activating mitogen‐activated protein kinases (MAPKs) and the nuclear factor ( NF )‐ κB . MAPKs belong to a large family of serine/threonine‐specific kinases including c‐Jun N‐terminal kinase (JNK), ERK and P38 that are demonstrated to be associated with myocardial dysfunction, hypertrophy, fibrosis, and heart failure . The activation of the MAPK signal pathways is also involved in the pathogenesis of diabetic cardiomyopathy.…”

Section: Introductionmentioning

confidence: 99%

Deep sea minerals ameliorate diabetic‐induced inflammation via inhibition of TNFα signaling pathways

Day

et al. 2019

Environmental Toxicology

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It has been well‐documented that the consumption of deep sea water (DSW) has beneficial effects on myocardial hypertrophy and cardiac apoptosis induced by hypercholesterolemia. However, the molecular mechanisms for the anti‐inflammatory effects of DSW on diabetic cardiomyopathy are still largely unclear. The main purpose of this present study was to test the hypothesis that DSW exerts anti‐inflammatory effects through the suppression of the TNF‐α‐mediated signaling pathways. IP injection of streptozotocin (STZ) at the dose of 65 mg/kg was used to establish a diabetes rat model. DSW mineral extracts that diluted in desalinated water were prepared in three different dosages and administered to the rats through gavages for 4 weeks. These dosages are DSW‐1X (equivalent to 37 mg Mg2+/kg/day), 2X (equivalent to 74 mg Mg2+/kg/day) and 3X (equivalent to 111 mg Mg2+ mg/kg/day). Immunofluorescence staining and Western blot showed that the protein expression level of TNF‐α was markedly higher in the STZ‐induced diabetic rat hearts than in the control group. Consequently, the phosphorylation levels of the TNF‐α‐modulated downstream signaling molecules and P38 mitogen‐activated protein kinases (MAPKs) were notably elevated in heart tissues of STZ‐induced diabetes. These higher phosphorylation levels subsequently upregulated NF‐κB‐modulated inflammatory mediators, such as cyclooxygenase (COX)‐II and inducible nitric oxide synthase (iNOS). However, treatment with DSW as well as MgSO4, the main mineral in DSW, significantly reversed all the alterations. These findings suggest that DSW has potential as a therapeutic agent for preventing diabetes‐related cardiovascular diseases.

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Mangiferin protect myocardial insults through modulation of MAPK/TGF-β pathways

Cited by 48 publications

References 31 publications

Protective effect of mangiferin on myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats: role of AGE-RAGE/MAPK pathways

Protective effect of mangiferin on myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats: role of AGE-RAGE/MAPK pathways

Mangiferin: Possible uses in the prevention and treatment of mixed osteoarthritic pain

Deep sea minerals ameliorate diabetic‐induced inflammation via inhibition of TNFα signaling pathways

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