Gastroprotective effects of diosgenin against HCl/ethanol-induced gastric mucosal injury through suppression of NF-κβ and myeloperoxidase activities

Zhao, Hengfang; Zhang, Xiaoyan; Zhang, Bojing; Qu, Xiaoyuan

doi:10.1515/biol-2021-0075

Cited by 10 publications

(9 citation statements)

References 30 publications

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“…It was demonstrated that oxidative stress could trigger neuronal damage in the hippocampus tissues of the brain, which is the vital pathological mechanism of neurodegenerative diseases, including AD[ 27 ]. Recently, the findings of the in vitro study certified that extracellular magnesium concentration could act as a regulator that effectively influenced the level of MDA, a pathological marker closely associated with oxidative stress damage[ 13 , 14 ]. Several researches indicated that MgT could elevate the level of brain magnesium via oral administration[ 10 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…Although MgT exhibits a protective effect against synaptic damage in an AD mouse model[ 11 ], its effects on oxidative stress and hippocampal neuronal damage remain unexplored. It has been recently confirmed that magnesium has an inhibitory effect against oxidative-stress-related malondialdehyde (MDA) in vitro [ 13 , 14 ]; therefore, it has become of interest to investigate whether MgT is capable of suppressing oxidative stress damage in vivo . Therefore, this research explored the potential protective effects of MgT against oxidative stress and neuronal injury in Aβ 25-35 -treated HT22 cells and in APPswe/PS1dE9 (APP/PS1) mouse hippocampus.…”

Section: Introductionmentioning

confidence: 99%

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Magnesium-L-threonate exhibited a neuroprotective effect against oxidative stress damage in HT22 cells and Alzheimer’s disease mouse model

Xiong¹,

Ruan²,

Zhao³

et al. 2022

WJP

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BACKGROUND Oxidative stress results in the production of excess reactive oxygen species (ROS) and triggers hippocampal neuronal damage as well as occupies a key role in the pathological mechanisms of neurodegenerative disorders such as Alzheimer’s disease (AD). A recent study confirmed that magnesium had an inhibitory effect against oxidative stress-related malondialdehyde in vitro . However, whether Magnesium-L-threonate (MgT) is capable of suppressing oxidative stress damage in amyloid β (Aβ) 25-35 -treated HT22 cells and the AD mouse model still remains to be investigated. AIM To explore the neuroprotective effect of MgT against oxidative stress injury in vitro and in vivo , and investigate the mechanism. METHODS Aβ 25-35 -induced HT22 cells were preconditioned with MgT for 12 h. APPswe/PS1dE9 (APP/PS1) mice were orally administered with MgT daily for 3 mo. After MgT treatment, the viability of Aβ 25-35 -treated HT22 cells was determined via conducting cell counting kit-8 test and the cognition of APP/PS1 mice was measured through the Morris Water Maze. Flow cytometry experiments were applied to assess the ROS levels of HT22 cells and measure the apoptosis rate of HT22 cells or hippocampal neurons. Expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X (Bax), hypoxia-inducible factor (HIF)-1α, NADPH oxidase (NOX) 4, Aβ 1-42 and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathway proteins was quantified by Western blot. RESULTS In vitro data confirmed that Aβ 25–35 -induced HT22 cells had a significantly lower cell viability, higher ROS level and higher apoptosis rates compared with those of control cells (all P < 0.001). MgT prevented the Aβ 25-35 -triggered oxidative stress damage by elevating viability and decreasing ROS formation and apoptosis of HT22 cells (all P < 0.001). APP/PS1 mice exhibited worse cognitive performance and higher apoptosis rate of hippocampal neurons than wild-type (WT) mice (all P < 0.01). Meanwhile, significant higher expression of Aβ 1-42 and NOX4 proteins was detected in APP/PS1 mice than those of WT mice (both P < 0.01). MgT also ameliorated the cognitive deficit, suppressed the apoptosis of hippocampal neuron and downregulated the expression of Aβ 1-42 and NOX4 proteins in APP/PS1 mouse (all P < 0.05). Moreover, MgT intervention significantly downregulated HIF-1α and Bax, upregulated Bcl-2 and activated the PI3K/Akt pathway both in vitro and in vivo ...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Magnesium-L-threonate exhibited a neuroprotective effect against oxidative stress damage in HT22 cells and Alzheimer’s disease mouse model

Xiong¹,

Ruan²,

Zhao³

et al. 2022

WJP

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“…ROS-activated lipid peroxidation is caused by a process in which free radicals interact with cell membranes to produce lipid peroxides, such as MDA. The level of MDA can indicate infiltration of neutrophils into gastric mucosal tissues [ 38 , 44 ]. In this study, the histopathological analysis showed abundant inflammatory cell infiltration into the damaged rat gastric tissues after ethanol exposure.…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective and Antioxidative Effects of the Traditional Thai Polyherbal Formula Phy-Blica-D against Ethanol-Induced Gastric Ulcers in Rats

et al. 2021

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Phy-Blica-D is a traditional Thai polyherbal formula that has reduced oxidative stress in non-communicable diseases. However, evidence supporting the gastroprotective effects of Phy-Blica-D has not been previously reported. Therefore, this study aimed to evaluate the gastroprotective effects of Phy-Blica-D against gastric ulcers in rats and investigate the potential underlying mechanism. To estimate the possible mechanisms of action, we examined the levels of oxidative stress markers, such as reactive oxygen species (ROS) and malondialdehyde (MDA), as well as antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH). According to our results, rats treated with only 80% ethanol (vehicle group) exhibited significant increases in their ulcer area and ulcer index (UI). Moreover, the levels of ROS and MDA markedly increased in the vehicle group compared with the normal control group. Daily oral administration of Phy-Blica-D (500 and 1000 mg/kg) for 7 days not only significantly decreased the ulcer area and UI, but also remarkably decreased the ROS and MDA levels in gastric tissue. Gastric ulcers induced by ethanol had significantly decreased antioxidant enzyme activities (CAT and SOD) and non-enzymatic antioxidant (GSH), whereas pretreatment with Phy-Blica-D significantly improved the activities of CAT, SOD, and GSH. Moreover, after exposure to ethanol, the rats exhibited a significantly increased level of inducible nitric oxide synthase (iNOS), which was reduced after treatment with Phy-Blica-D. These findings suggest that Phy-Blica-D potentially exerts its gastroprotective effects by suppressing oxidative stress and stimulating antioxidant enzymes, which is one of the causes of destruction of cell membranes, and it is involved in the pathogenesis of acute gastric ulcers induced by ethanol.

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“…42 This transition to an oxidative state is caused by the release of hydroperoxide radicals and superoxide anions, and their increase leads to oxidative stress, which can be seen as an increase in MDA levels. 43 In this study, oral alcohol markedly increased MDA levels and reduced SOD activity (Figure 8A and B), supporting the notion that oxidative stress plays an essential role in the pathogenesis of alcohol-induced gastric injury. 9 Interestingly, OME, BSP, mixture, and OME-BSP NPs can decrease the MDA levels and increase the SOD activity to some extent, and OME-BSP NPs were more effective on the antioxidative activities than physical mixtures of OME and BSP during the MDA test (P < 0.01).…”

Section: Ome-bsp Nps Can Alleviate the Cell Apoptosis Induced By Ethanolmentioning

confidence: 93%

Bletilla striata Polysaccharide Nanoparticles Improved the Therapeutic Efficacy of Omeprazole on the Rat Gastric Ulcer Induced by Ethanol

Jing

Yang

et al. 2023

Mol. Pharmaceutics

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Gastric ulcers are a common clinical presentation affecting anyone, regardless of their age or gender. Nanoparticles (NPs) containing Bletilla striata polysaccharide (BSP) and omeprazole (OME) were investigated in the study for their therapeutic effect on gastric ulcers. Ethanol-induced gastric ulcers in rats (240 ± 30 g) were established. Our OME-BSP NPs were more stable than free OME in the acidic environment and can increase the absorption of OME in rat stomach, which was confirmed by in situ gastric absorption and distribution experiments. The extended blood circulation of OME-BSP NPs was also observed in rats with gastric ulcer. More importantly, OME-BSP NPs not only decreased the area of gastric ulcer and inhibited gastric acid secretion but also reversed gastric tissue damage and cell apoptosis, as revealed by HE and TUNEL staining. Subsequent SOD, MDA, PGE2, IL-6, and TNF-α tests further verified the superiority of OME-BSP NPs against rat gastric ulcer, which properly originated from superior antioxidant and anti-inflammatory effects. As a result, our OME-BSP NPs’ drug delivery system improved the stability and absorption of OME in the rat stomach and achieved targeted treatment of gastric ulcers.

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Gastroprotective effects of diosgenin against HCl/ethanol-induced gastric mucosal injury through suppression of NF-κβ and myeloperoxidase activities

Cited by 10 publications

References 30 publications

Magnesium-L-threonate exhibited a neuroprotective effect against oxidative stress damage in HT22 cells and Alzheimer’s disease mouse model

Magnesium-L-threonate exhibited a neuroprotective effect against oxidative stress damage in HT22 cells and Alzheimer’s disease mouse model

Gastroprotective and Antioxidative Effects of the Traditional Thai Polyherbal Formula Phy-Blica-D against Ethanol-Induced Gastric Ulcers in Rats

Bletilla striata Polysaccharide Nanoparticles Improved the Therapeutic Efficacy of Omeprazole on the Rat Gastric Ulcer Induced by Ethanol

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