The protective effect of procyanidin against LPS-induced acute gut injury by the regulations of oxidative state

Wu, Qiu Jue; Wang, Yu Qin; Qi, Yan

doi:10.1186/s40064-016-3306-y

Cited by 21 publications

(9 citation statements)

References 33 publications

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“…SOD activity showed a significant decrease after 72 hours of LPS treatment which was observed in broilers treated with 0.5 mg/ml LPS attributing to disturbance in antioxidant defense system [43].…”

Section: Discussionmentioning

confidence: 91%

Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

Halawa

El‐Adl

Hamed

et al. 2018

JVHC

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Lipopolysaccharide (LPS) is a component of the outer membrane of gram negative bacteria. LPS challenging allows switching transcription of proinflammatory cytokines on via over stimulation of Toll-like receptors (TLRs) signaling pathway with subsequent pathogenic inflammatory response. We investigated the possible reproductive toxicity of LPS in male Wister albino rats. Oxidative stress markers, antioxidant status and caspase-3 activity were analyzed in testicular tissues of rats exposed to either saline or LPS (4 mg/kg BW, ip; 0.18 of the LD 50 ). The samples were collected at 6 h and 72 h after injection of LPS. A significant reduction in testicular reduced glutathione (GSH), glutathione-S-transferase (GST) and superoxide dismutase (SOD) was observed at 72 h compared to control group. Total antioxidant capacity was decreased at 6 h with additional significant reduction at 72 h. Catalase activity was reduced significantly at both 6 and 72 h. Malondialdehyde (MDA) was increased (P ≤ 0.05) in LPS injected rats without variation between 6 and 72 h. A significant increase in nitric oxide (NO) was observed at 72 h after injection. A time-dependent increase in LPS-treated groups was observed in the concentration of caspase-3.Histopathological analysis revealed degenerative changes and necrosis of seminiferous tubules after 6 h with further accumulation of eosinophilic edematous transudate in its lumen after 72 h. In conclusion, by increasing time of exposure, LPS induced lipid peroxidation, oxidative stress, reduced testicular antioxidant capacity and encouraged testicular apoptosis which could be possible mechanisms for impairment of testicular function.

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Section: Discussionmentioning

confidence: 91%

Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

Halawa

El‐Adl

Hamed

et al. 2018

JVHC

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“…Increased oxidative stress is associated with increased mortality during sepsis. Previous studies showed that LPS exposure could cause oxidative stress in the gut, and antioxidant administration was suggested as a potential therapy for protecting against organ injuries in experimental studies [18,19]. However, treatment with antioxidant in sepsis patients could not be effective.…”

Section: Discussionmentioning

confidence: 99%

MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

Zhang

Zhou

et al. 2020

Mediators of Inflammation

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Background. Gut barrier dysfunction with alterant mucosal permeability during sepsis is a challenge problem in clinical practice. Intestinal epithelial cells (IECs) are strongly involved in mucosal oxidative stress and inflammatory response. The current study aimed at investigating the effect of MitoQ, a mitochondrial targeted antioxidant, in the treatment of intestinal injury and its potential mechanism during sepsis. Methods. 30 minutes before sepsis induction by lipopolysaccharide (LPS) treatment, mice were treated with MitoQ. Intestinal histopathology, mucosal permeability, inflammatory cytokines, and mucosal barrier proteins were evaluated in the present study. Results. MitoQ pretreatment significantly decreased the levels of plasma diamine oxidase, D-lactate, and intestinal histological damage and markedly restored the levels of tight junction proteins (ZO-1 and occludin) following LPS challenge. Furthermore, MitoQ inhibited the LPS-induced intestinal oxidative stress and inflammatory response, evidenced by increased levels of intestinal superoxide dismutase and glutathione, and decreased levels of intestinal IL-1, IL-6, TNF-α, and nitric oxide levels. Mechanically, we found that MitoQ inhibited the oxidative stress via activating nuclear factor E2-related factor 2 (Nrf2) signaling pathway and its downstream antioxidant genes, including HO-1, NQO-1, and GCLM. Conclusions. MitoQ exerts antioxidative and anti-inflammatory effects against sepsis-associated gut barrier injury by promoting Nrf2 signaling pathway.

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“…The results of the aforementioned studies suggest that PB2 displays protective effects in HUVECs ( 26 ). Procyanidin protects against glycated low-density lipoprotein-induced apoptosis and LPS-induced acute gut injury via regulating the oxidative state ( 28 , 29 ). However, the mechanism underlying the anti-inflammatory and antiapoptotic effects of PB2 is not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Procyanidin B2 inhibits lipopolysaccharide‑induced apoptosis by suppressing the Bcl‑2/Bax and NF‑κB signalling pathways in human umbilical vein endothelial cells

et al. 2021

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Human umbilical vein endothelial cells (HUVECs) serve a critical role in maintaining normal vascular function. Lipopolysaccharide (LPS), which is released from pathogenic bacteria in the blood, induces HUVEC apoptosis and injury to cause vascular dysfunction and infectious vascular diseases. Procyanidin B2 (PB2) possesses numerous functions, including antioxidant, antitumor, anti-inflammatory and antiapoptosis effects, but the molecular mechanism is not completely understood. The present study investigated the effects of PB2 on LPS-induced cytotoxicity and apoptosis in HUVECs, as well as the underlying mechanisms. The effects of PB2 on LPS-mediated alterations to cytotoxicity, mitochondrial membrane potential, apoptosis were assessed by performing Cell Counting Kit-8, JC-1 fluorescence, Hoechst 33258 staining assays, respectively. IL-1β, IL-6 and TNF-α mRNA expression and protein levels were measured by performing reverse transcription-quantitative PCR and ELISAs, respectively. Bcl-2, Bax, cleaved caspase-3, cleaved caspase-7, cleaved caspase-9, phosphorylated (p)-IκB-α, p-IκB-β, p-NF-κB-p65 and total NF-κB p65 protein expression levels were determined via western blotting. NF-κB p65 nuclear translocation was assessed via immunofluorescence. PB2 pretreatment markedly attenuated LPS-induced cytotoxicity and apoptosis in HUVECs. PB2 also significantly downregulated the expression levels of IL-1β, IL-6, TNF-α, Bax, cleaved caspase-3, cleaved caspase-7, cleaved caspase-9 and p-NF-κB-p65, but upregulated the expression levels of Bcl-2, p-IκB-α and p-IκB-β in LPS-induced HUVECs. Moreover, PB2 markedly inhibited LPS-induced NF-κB p65 nuclear translocation in HUVECs. The results suggested that the potential molecular mechanism underlying PB2 was associated with the Bax/Bcl-2 and NF-κB signalling pathways. Therefore, PB2 may serve as a useful therapeutic for infectious vascular diseases.

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The protective effect of procyanidin against LPS-induced acute gut injury by the regulations of oxidative state

Cited by 21 publications

References 33 publications

Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

Procyanidin B2 inhibits lipopolysaccharide‑induced apoptosis by suppressing the Bcl‑2/Bax and NF‑κB signalling pathways in human umbilical vein endothelial cells

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