Dietary pomegranate supplement alleviates murine pancreatitis by modulating Nrf2-p21 interaction and controlling apoptosis to survival switch

Gupta, P. C. Sen; Choudhury, Sumana; Ghosh, Sayan; Mukherjee, Sudeshna; Chowdhury, Olivia; Sain, Arindam; Chattopadhyay, Sreya

doi:10.1016/j.jnutbio.2018.12.009

Cited by 17 publications

(5 citation statements)

References 33 publications

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“…especially the expression of several members of the Bcl-2 family (Binju et al, 2019). The nuclear fraction of Nrf2 is able to bind to the Bcl-2 promoter and activate an anti-apoptotic program (Gupta et al, 2019). In addition, we demonstrated that cell apoptosis is induced by As(III) through activation of the mitochondrial pathway (Figures 3, 8).…”

Section: Discussionmentioning

confidence: 65%

“…p53 is a tumor suppressor protein that promotes the apoptotic process ( Jiang and Rusling, 2019 ; Silva-Adaya et al., 2020 ) and directly regulate the activity of the pro-apoptotic protein Bax, which further facilitates mitochondrial membrane permeabilization and apoptosis, especially the expression of several members of the Bcl-2 family ( Binju et al., 2019 ). The nuclear fraction of Nrf2 is able to bind to the Bcl-2 promoter and activate an anti-apoptotic program ( Gupta et al., 2019 ). In addition, we demonstrated that cell apoptosis is induced by As(III) through activation of the mitochondrial pathway ( Figures 3 , 8 ).…”

Section: Discussionmentioning

confidence: 99%

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Ursodeoxycholic Acid Protects Against Arsenic Induced Hepatotoxicity by the Nrf2 Signaling Pathway

Zhang

et al. 2020

Front. Pharmacol.

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Arsenic is ubiquitous toxic metalloid responsible for many human diseases all over the world. Contrastingly, Ursodeoxycholic acid (UDCA) has been suggested as efficient antioxidant in various liver diseases. However, there are no reports of the effects of UDCA on arsenious acid [As(III)]-induced hepatotoxicity. The objective of this study is to elucidate the protective actions of UDCA on As(III)-induced hepatotoxicity and explore its controlling role in biomolecular mechanisms in vivo and in vitro. The remarkable liver damage induced by As(III) was ameliorated by treatment with UDCA, as reflected by reduced histopathological changes of liver and elevation of serum AST, ALT levels. UDCA play a critical role in stabilization of cellular membrane potential, inhibition of apoptosis and LDH leakage in LO2 cells. Meanwhile, the activities of SOD, CAT and GSH-Px and the level of TSH, GSH were enhanced with UDCA administration, while the accumulations of intracellular ROS, MDA and rate of GSSG/GSH were decreased in vivo and in vitro. Further study disclosed that UDCA significantly inhibited As(III)-induced apoptosis through increasing the expression of Bcl-2 and decreasing the expression of Bax, p53, Cyt C, Cleaved caspase-3 and 9. Moreover, UDCA promoted the expression of nuclear Nrf2, HO-1, and NQO1, although arsenic regulated nuclear translocation of Nrf2 positively. When Nrf2 was silenced, the protective effect of UDCA was abolished. Collectively, the results of this study showed that UDCA protects hepatocytes antagonize As(III)-induced cytotoxicity, and its mechanism may be related to activation of Nrf2 signaling.

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Ursodeoxycholic Acid Protects Against Arsenic Induced Hepatotoxicity by the Nrf2 Signaling Pathway

Zhang

et al. 2020

Front. Pharmacol.

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“…The authors mainly focus on Nrf2 signaling, as a canonical antioxidative agent, and discuss in what manner it is influenced by various exogenous antioxidants. Unfortunately, only a few studies examined whether the observed antioxidative effects and mitigation of symptoms of AP and CP result from an exclusive stimulation of Nrf2 pathway (Xu et al 2020;Gupta et al 2019;Chen 2020;Lee et al 2022). Furthermore, the impact of other signaling pathways on oxidative damage of pancreas is much less evaluated compared to Nrf2 signaling.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, our research of literature revealed that Nrf2 signaling was restored by several exogenous antioxidants, such as high-dose vitamin C, pomegranate extract, Tanshinone IIA (the main active component of red sage), and lycopene. However, this effect was abolished when inhibitors of Nrf2 were used (Xu et al 2020;Gupta et al 2019;Chen 2020;Lee et al 2022). Nrf2 pathway may be influenced by several other factors, including melatonin, hepatocyte growth factor, vinpocetine, borneol, visnagin, chitosan oligosaccharides, or flavonoids derived from Coreopsis tinctoria nuts (Jung et al 2010;Palestino-Dominguez et al 2018;Abdelzaher et al 2021;Bansod et al 2021;Pasari 2019;Mei, et al 2021;Du, et al 2018).…”

Section: Keap1/nrf2/are Pathwaymentioning

confidence: 99%

Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis — a systematic review

Burzyński

Fichna

Tarasiuk

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Acute pancreatitis (AP) and chronic pancreatitis (CP) are debilitating diseases of gastrointestinal tract and constitute great threat for human health in high-income countries. Recent studies emphasize the impact of oxidative stress on development of these pathologies, and numerous authors evaluate the effect of the antioxidant therapy on the course of AP and CP. Though several antioxidative agents were discovered in the past decades, vitamins remain canonical antioxidants. Despite the fact that vitamin A is known for its antioxidative effect, there is little data about the impact of vitamin A on oxidative stress in the pathogenesis of AP and CP. The scope of the review is to evaluate molecular targets for vitamin A, which may be involved in oxidative stress occurring in the course of AP and CP. Our research of available literature revealed that several mechanisms are responsible for attenuation of oxidative stress in AP and CP, including Nrf2, MAPK, AMPK, TLR3, and TLR4. Furthermore, these factors are at least partially expressed in vitamin A-dependent manner, though further investigations are required for elucidating in detail the role of vitamin A in defense against reactive oxygen species. Our review revealed that vitamin A might influence the expression of several molecular pathways involved in antioxidative defense and cytoprotection; thus, its administration during AP and CP may change the course of the disease.

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“…Systemic inflammation increases the burden on organs and aggravates the severity of AP, bringing a second blow to patients. In addition, intracellular ROS accumulation also aggravates AP injury [13]. AA has anti-inflammatory effects and inhibits various inflammatory reactions, such as skin inflammation and rheumatoid arthritis [6].…”

Section: Discussionmentioning

confidence: 99%

Abietic acid ameliorates pancreatic injury in acute pancreatitis by modulating MAPK pathway

Ye,

Wang,

Mao

et al. 2023

Trop. J. Pharm Res

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Purpose: To examine the effect of abietic acid (AA) in the treatment of acute pancreatitis (AP) in mice.Methods: C57BL/6J mice were randomly assigned to 4 groups: sham, AP, AP + 20 mg/kg AA, and AP + 40 mg/kg AA groups. To induce AP mouse model, the mice received intraperitoneal (IP) injections of cerulein. The extent of pancreatic tissue damage was evaluated by histological examination. Serum ALT, lipase, and amylase levels were determined by commercial kits while TUNEL assay was used to assess the apoptosis of pancreatic cells. The contents of Bax, Caspase-3, Bcl-2, p-ERK/ERK, p-JNK/JNK, and p-P38/P38 in pancreatic tissues were evaluated by western blot while the contents of IL-6, TNF-α, IL-1β, nitrite, MDA, and GSH in the tissues were evaluated by enzyme-linked immunosorbent assay (ELISA) kits.Results: AA relieved pancreatic damage and reduced ALT, lipase, and amylase levels in ceruleintreated AP mouse (p < 0.001). AA repressed apoptosis of pancreatic cells in cerulein-induced AP mouse, and inhibited oxidative stress and inflammatory response in the mice by reducing IL-6, TNF-α, IL-1β, nitrite, and MDA contents; it also enhanced the levels of GSH in the tissues (p < 0.001). In addition, AA inhibited MAPK pathway activity in the mice (p < 0.001).Conclusion: AA ameliorates pancreatic damage, pancreatic cell apoptosis, oxidative stress, and inflammation in cerulein-induced AP mouse by inhibiting MAPK pathway. This study offers a new potential drug for the management of AP and expands the relevant molecular regulatory mechanisms.

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Dietary pomegranate supplement alleviates murine pancreatitis by modulating Nrf2-p21 interaction and controlling apoptosis to survival switch

Cited by 17 publications

References 33 publications

Ursodeoxycholic Acid Protects Against Arsenic Induced Hepatotoxicity by the Nrf2 Signaling Pathway

Ursodeoxycholic Acid Protects Against Arsenic Induced Hepatotoxicity by the Nrf2 Signaling Pathway

Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis — a systematic review

Abietic acid ameliorates pancreatic injury in acute pancreatitis by modulating MAPK pathway

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