Vanillic acid retains redox status in HepG2 cells during hyperinsulinemic shock using the mitochondrial pathway

Mohan, Sreelekshmi; George, Genu; Raghu, Kozhiparambil Gopalan

doi:10.1016/j.fbio.2021.101016

Cited by 7 publications

(9 citation statements)

References 72 publications

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“…The reactive oxygen species (ROS) formation was estimated using DCFH‐DA fluorescent dye 22 . Briefly, DCFH‐DA was added (20 µM) to the cells, and incubated for 20 min at 37°C, then washed three times with HBSS and fluorescence intensity was measured using a microplate reader (Infinite® M200 PRO, Tecan Group Ltd; excitation/emission: 488/525 nm), then images were taken (Olympus IX 83).…”

Section: Methodsmentioning

confidence: 99%

Methylglyoxal induces ambience for cancer promotion in HepG2 cells via Warburg effect and promotes glycation

Sruthi

Raghu

2022

J of Cellular Biochemistry

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Methylglyoxal (MGO) is a toxic, highly reactive metabolite derived mainly from glucose and amino acids degradation. MGO is also one of the prime precursors for advanced glycation end products formation. The present research was performed to check whether MGO has any role in the promotion of cancer in HepG2 cells. For this, cells were incubated with MGO (50 µM) for 24 h and subjected to various analyses. Aminoguanidine (200 µM) was positive control. The various biochemical and protein expression studies, relevant to the MGO detoxification system, oxidative stress, and glycolysis were performed. MGO caused the reduction of expression of GLO 1 (27%) and GLO 2 (11%) causing weakening of the innate detoxification system. This is followed by an increase of RAGE (95%), AGEs or methylglyoxal adducts. We also observed hypoxia via estimation of oxygen consumption rate and surplus reactive oxygen species (ROS) (24%). To investigate the off‐target effect of MGO we checked its effect on glucose transport, and its associated proteins. Glucose uptake was found to increase (15%) significantly with overexpression of GLUT 1 (35%). We also found a significant increase of glycolytic enzymes such as hexokinase II, phosphofructokinase 1, and lactate dehydrogenase along with lactate production. Observation of surplus ROS and enhanced glycolysis led us to check the expression of HIF 1α which is their downstream signaling pathway. Interestingly HIF 1α was found to increase significantly (35%). It is known that enhanced glycolysis and oxidative stress are catalysts for the overexpression of HIF 1α which in turn creates an ambience for the promotion of cancer. Aminoguanidine was able to prevent the adverse effect of MGO partially. This is the first study to show the potential of MGO for the promotion of cancer in the non‐tumorigenic HepG2 cells via the Warburg effect and glycation.

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Section: Methodsmentioning

confidence: 99%

Methylglyoxal induces ambience for cancer promotion in HepG2 cells via Warburg effect and promotes glycation

Sruthi

Raghu

2022

J of Cellular Biochemistry

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“…Interestingly, the new evidence reported that hyperinsulinaemia alters the redox balance in HepG2 cells (hepatocellular carcinoma cell line) due to mitochondrial disorders, lipid peroxidation, and reduced levels of innate antioxidants. The results revealed that VA could contribute to maintaining mitochondria in terms of dynamics, biogenesis, bioenergetics, and integrity under conditions of hyperinsulinaemic shock 24 …”

Section: Vanillic Acidmentioning

confidence: 95%

“…The results revealed that VA could contribute to maintaining mitochondria in terms of dynamics, biogenesis, bioenergetics, and integrity under conditions of hyperinsulinaemic shock. 24 The outcomes of diverse studies have highlighted the other pharmacological potential of VA against nephrotoxicity, 82 asthma, 83 osteoarthritis, 17 periodontal disease, 84 inflammatory pain, 85 ulcerative colitis, 86 and polycystic ovary syndrome. 87 In addition to the disorders as mentioned above, pretreatment with VA could ameliorate cardiovascular dysfunction, including myocardial cell injury caused by drugs and ischaemia-reperfusion injury (IRI) in animal models.…”

Section: Vanillic Acidmentioning

confidence: 99%

“…[19][20][21][22] Numerous studies have revealed that VA therapy amends renal dysfunction, hyperglycaemia, lipid profile modifications, hepatotoxicity and metastasis through its antioxidant activity. 21,23,24 In addition, experimental studies have verified the advantageous effects of this antioxidant on cardiovascular disorders such as CTX and MIRI. [25][26][27] VA could decline cardiomyocytes toxicity, apoptosis and pro-inflammatory mediators, and enhance the activity of antioxidant enzymes comprising superoxide dismutase) SOD(and catalase (CAT).…”

Section: Introductionmentioning

confidence: 97%

“…VA has also been demonstrated to have pharmacological potential against multiple diseases including diabetes, cancer, hepatic disorders, hypertension and other pathologic conditions 19–22 . Numerous studies have revealed that VA therapy amends renal dysfunction, hyperglycaemia, lipid profile modifications, hepatotoxicity and metastasis through its antioxidant activity 21,23,24 . In addition, experimental studies have verified the advantageous effects of this antioxidant on cardiovascular disorders such as CTX and MIRI 25–27 .…”

Section: Introductionmentioning

confidence: 99%

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Cardioprotective potential of vanillic acid

Yalameha

Nejabati

Nouri

2022

Clin Exp Pharma Physio

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Nowadays, cardiovascular diseases (CVDs) are a global threat to public health, accounting for almost one‐third of all deaths worldwide. One of the key mechanistic pathways contributing to the development of CVDs, including cardiotoxicity (CTX) and myocardial ischaemia–reperfusion injury (MIRI) is oxidative stress (OS). Increased generation of reactive oxygen species (ROS) is closely associated with decreased antioxidant capacity and mitochondrial dysfunction. Currently, despite the availability of modern pharmaceuticals, dietary‐derived antioxidants are becoming more popular in developed societies to delay the progression of CVDs. One of the antioxidants derived from herbs, fruits, whole grains, juices, beers, and wines is vanillic acid (VA), which, as a phenolic compound, possesses different therapeutic properties, including cardioprotective. Based on experimental evidence, VA improves mitochondrial function as a result of the reduction in ROS production, aggravates antioxidative status, scavenges free radicals, and reduces levels of lipid peroxidation, thereby decreasing cardiac dysfunction, in particular CTX and MIRI. Considering the role of OS in the pathophysiology of CVDs, the purpose of this study is to comprehensively address recent evidence on the antioxidant importance of VA in the cardiovascular system.

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Hesperidin, vanillic acid, and sinapic acid attenuate atorvastatin‐induced mitochondrial dysfunction via inhibition of mitochondrial swelling and maintenance of mitochondrial function in pancreas isolated mitochondria

Salimi,

Khezri,

Vahabzadeh

et al. 2024

Drug Development Research

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It has been reported that lipophilic statins such as atorvastatin can more readily penetrate into β‐cells and reach the mitochondria, resulting in mitochondrial dysfunction, oxidative stress, decrease in insulin release. Many studies have shown that natural products can protect mitochondrial dysfunction induced by drug in different tissue. We aimed to explore mitochondrial protection potency of hesperidin, vanillic acid, and sinapic acid as natural compounds against mitochondrial dysfunction induced by atorvastatin in pancreas isolated mitochondria. Mitochondria were isolated form rat pancreas and directly treated with toxic concentration of atorvastatin (500 µM) in presence of various concentrations hesperidin, vanillic acid, and sinapic acid (1, 10, and 100 µM) separately. Mitochondrial toxicity parameters such as the reactive oxygen species (ROS) formation, succinate dehydrogenases (SDH) activity, mitochondrial swelling, depletion of glutathione (GSH), mitochondrial membrane potential (MMP) collapse, and malondialdehyde (MDA) production were measured. Our findings demonstrated that atorvastatin directly induced mitochondrial toxicity at concentration of 500 μM and higher in pancreatic mitochondria. Except MDA, atorvastatin caused significantly reduction in SDH activity, mitochondrial swelling, ROS formation, depletion of GSH, and collapse of MMP. While, our data showed that all three protective compounds at low concentrations ameliorated atorvastatin‐induced mitochondrial dysfunction with the increase of SDH activity, improvement of mitochondrial swelling, MMP collapse and mitochondrial GSH, and reduction of ROS formation. We can conclude that hesperidin, vanillic acid, and sinapic acid can directly reverse the toxic of atorvastatin in rat pancreas isolated mitochondria, which may be beneficial for protection against diabetogenic‐induced mitochondrial dysfunction in pancreatic β‐cells.

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Vanillic acid retains redox status in HepG2 cells during hyperinsulinemic shock using the mitochondrial pathway

Cited by 7 publications

References 72 publications

Methylglyoxal induces ambience for cancer promotion in HepG2 cells via Warburg effect and promotes glycation

Methylglyoxal induces ambience for cancer promotion in HepG2 cells via Warburg effect and promotes glycation

Cardioprotective potential of vanillic acid

Hesperidin, vanillic acid, and sinapic acid attenuate atorvastatin‐induced mitochondrial dysfunction via inhibition of mitochondrial swelling and maintenance of mitochondrial function in pancreas isolated mitochondria

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