Therapeutic Potential of Vanillin and its Main Metabolites to Regulate the Inflammatory Response and Oxidative Stress

Bezerra-Filho, Carlos S. M.; Barboza, Joice Nascimento; Souza, Marilia T.S.; Sabry, Peter; Ismail, Nasser S. M.; Sousa, Damião Pergentino de

doi:10.2174/1389557519666190312164355

Cited by 41 publications

(31 citation statements)

References 75 publications

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“…Both agents act as free radical scavengers, reduce generation of ROS, maintain endogenous antioxidant capacity, prevent lipid peroxidation of biomembranes and decrease the production of inflammatory cytokines. 12,13 This is consistent with the present investigation which revealed that treatment with NGN, VLN and NGN + VLN caused significant decrements of MDA, NF-κB p65,TNF-α and IL-1β and significant preservation of GSH and CAT in the pancreas of cadmium-challenged rats. The current work also demonstrated that NGN, VLN and NGN + VLN significantly decreased Bax/Bcl-2 ratio and caspase-3 activation in pancreas of rats challenged with cadmium and thus offered protection against cell apoptosis.…”

Section: Discussionsupporting

confidence: 92%

“…Both NGN and VLN have antioxidant, anti-inflammatory, anti-apoptotic and anti-carcinogenic activities. 12,13 It was reported in the literature that NGN and VLN significantly protected against streptozotocininduced pancreatic β-cell injury and diabetes mellitus. [14][15][16] In addition, NGN mitigated acute pancreatitis induced by caerulein and L-arginine in mice.…”

Section: Introductionmentioning

confidence: 98%

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Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways

Fouad¹,

Amin²,

Ahmed³

2020

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Chemicals NGN, VLN and CdCl 2 were purchased from Sigma-Aldrich, USA. VLN and CdCl 2 were ABSTRACT Background: Cadmium can induce pancreatic injury via oxidative stress, inflammation and apoptosis. Naringenin (NGN) and vanillin (VLN) exert antioxidant, anti-inflammatory, and antiapoptotic effects. Objective: The likely ameliorative effects of NGN, VLN and their combination were studied in rats exposed to cadmium-induced pancreatic injury. Materials and Methods: Rats received NGN (50 mg/kg/day, p.o.), VLN (100 mg/ kg/day, p.o.), or NGN + VLN for 7 days and one injection of CdCl 2 (2 mg/kg, i.p.) on the 6 th day. Results: Cadmium significantly lowered serum amylase and insulin levels. Cadmium also caused significant increments of malondialdehyde, tumor necrosis factor-α, interleukin-1β, nuclear factor-κB p65, Bax/Bcl-2 ratio and phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 mitogen-activated protein kinases (MAPKs) and significant decrements of reduced glutathione and catalase in the pancreas of rats received CdCl 2. Additionally, CdCl 2 caused marked histopathological necrosis and significantly increased caspase-3 expression in pancreatic tissue. The cadmium-induced biochemical, histopathological and immunohistochemical changes were significantly ameliorated by NGN, VLN and NGN + VLN. However, NGN + VLN caused more significant ameliorative effects than did NGN and VLN alone. Conclusion: NGN, VLN and NGN + VLN afforded significant protection of pancreas in rats exposed to cadmium insult through modulation of JNK and p38 MAPK pathways and inhibition of oxidative stress, inflammation and apoptosis.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways

Fouad¹,

Amin²,

Ahmed³

2020

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“…Oxidative stress induction and a life-threatening ROS production represent the main mechanism by which doxo generally induces cardiotoxicity [ 7 ]. In the same way, vanillin exerts its beneficial properties exactly providing an antioxidant action [ 37 , 39 , 44 ]. With the purpose of investigating the molecular mechanism associated with the beneficial effect of vanillin in preventing doxo-induced cardiotoxicity, we analyzed the ability of vanillin to affect the oxidative stress in H9c2 cells exposed to doxo.…”

Section: Resultsmentioning

confidence: 99%

“…Among the others, vanillin, the major component of vanilla bean extract, is one of the main and stable degradation products of curcumin [ 34 , 35 , 36 ]. Vanillin is a widely known antioxidative, anti-apoptotic, anti-inflammatory, neuroprotective and anticancer compound [ 37 , 38 , 39 ]. However, no data are currently available concerning the vanillin-mediated cardioprotective features.…”

Section: Introductionmentioning

confidence: 99%

Vanillin Prevents Doxorubicin-Induced Apoptosis and Oxidative Stress in Rat H9c2 Cardiomyocytes

et al. 2020

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Doxorubicin (doxo) is an effective anticancer compound in several tumor types. However, as a consequence of oxidative stress induction and ROS overproduction, its high cardiotoxicity demands urgent attention. Vanillin possesses antioxidant, antiproliferative, antidepressant and anti-glycating properties. Therefore, we investigated the potential vanillin protective effects against doxo-induced cardiotoxicity in H9c2 cells. Using multiparametric approach, we demonstrated that vanillin restored both cell viability and damage in response to doxo exposure. Contextually, vanillin decreased sub-G1 appearance and caspase-3 and PARP1 activation, reducing the doxo-related apoptosis induction. From a mechanistic point of view, vanillin hindered doxo-induced ROS accumulation and impaired the ERK phosphorylation. Notably, besides the cardioprotective effects, vanillin did not counteract the doxo effectiveness in osteosarcoma cells. Taken together, our results suggest that vanillin ameliorates doxo-induced toxicity in H9c2 cells, opening new avenues for developing alternative therapeutic approaches to prevent the anthracycline-related cardiotoxicity and to improve the long-term outcome of antineoplastic treatment.

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“…4-pyridoxic acid is a metabolite of vitamin B6, and dehydroascorbic acid is the product of ascorbic acid reacting with ROS. These compounds, including vitamin B6, ascorbic acid and vanillin are antioxidants 30 , and we speculate that organisms possess multiple endogenous defense mechanisms against ROS caused by PQ.…”

Section: Discussionmentioning

confidence: 89%

Toxicology of paraquat and pharmacology of the protective effect of 5-hydroxy-1-methylhydantoin on lung injury caused by paraquat based on metabolomics

Gao

Yuan

et al. 2020

Sci Rep

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Paraquat (PQ) is a non-selective herbicide and is exceedingly toxic to humans. The mechanism of PQ toxicity is very complex and has not been clearly defined. There is no specific antidote for PQ poisoning. 5-hydroxy-1-methylhydantoin (HMH) is an intrinsic antioxidant and can protect against renal damage caused by PQ. The mechanism of PQ toxicology and the possible effects of HMH on PQ-induced lung injury were determined in this study. It was found that PQ decreased superoxide dismutase (SOD) activity and elevated the level of malondialdehyde (MDA), while HMH elevated SOD activity and decreased the level of MDA. Based on metabolomics, the citrate cycle, glutathione metabolism, taurine and hypotaurine metabolism, regulation of lipolysis in adipocytes, inflammatory mediator regulation of tRp channels, purine and pyrimidine metabolism, aldosterone synthesis and secretion, and phenylalanine metabolism were changed in the PQ group. Compared with the PQ group, the levels of N-acetyl-l-aspartic acid, L-glutamic acid, L-aspartic acid, mesaconic acid, adenosine 5′ monophosphate, methylmalonic acid, cytidine, phosphonoacetic acid, hypotaurine, glutathione (reduced) and cysteinylglycine increased, while the levels of corticosterone, xanthine, citric acid, prostaglandin G2, 4-pyridoxic acid and succinyl proline decreased in the HMH group. These metabolites revealed that HMH can alleviate inflammation caused by PQ and elevate the activity of intrinsic antioxidants. In conclusion, our results revealed PQ toxicology and the pharmacology underlying the protective effect of HMH on lung injury due to PQ. Toxicity caused by PQ results in lipid peroxidation and an increase in reactive oxygen species (RoS), nitric oxide (no), damage to the biliary system, gastrointestinal system and nervous system, in addition to lungs, kidneys, and the liver. HMH is a good antioxidant and protects against lung injury caused by PQ. In summary, HMH efficiently reduced PQ-induced lung injury in mice. Paraquat (PQ, 1,1′-dimethyl-4-4′-bipyridinium dichloride) is a highly toxic quaternary ammonium herbicide widely used in agriculture. The mortality rate of PQ poisoning is as high as 60-80%, mainly due to acute lung injury and progressive pulmonary fibrosis 1-3. Moreover, there is no specific antidote for PQ poisoning. Following PQ poisoning, the lungs are the main target organs, and the redox reaction occurs after the uptake of PQ in the lungs, which interferes with mitochondrial electron transfer, generates a large number of oxygen free radicals, and induces lipid peroxidation injury 2. PQ enters the body and is excreted in the form of a prototype in the kidney, where the concentration is highest, resulting in impaired renal function. PQ cannot be excreted normally and further accumulates in the body; thus, involving other organs such as the liver, heart and lung, resulting in multiple organ failure 2. Creatinine is a degradation product of creatine, which is degraded at a constant rate. When renal function is impaired, large amounts of creatinine are acc...

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Therapeutic Potential of Vanillin and its Main Metabolites to Regulate the Inflammatory Response and Oxidative Stress

Cited by 41 publications

References 75 publications

Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways

Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways

Vanillin Prevents Doxorubicin-Induced Apoptosis and Oxidative Stress in Rat H9c2 Cardiomyocytes

Toxicology of paraquat and pharmacology of the protective effect of 5-hydroxy-1-methylhydantoin on lung injury caused by paraquat based on metabolomics

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