Selenium-Rich Yeast protects against aluminum-induced peroxidation of lipide and inflammation in mice liver

Luo, Junchong; Li, Xiaowen; Li, Xinran; He, Yueqiu; Zhang, Mengdan; Cao, Changyu; Wang, Kai

doi:10.1007/s10534-018-0150-2

Cited by 24 publications

(12 citation statements)

References 40 publications

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“…[13][14][15] The preceding study has pointed out that Nrf2/HO-1 pathway is one of the most recognized signaling closely associated with oxidative and anti-oxidative balance. 16,17 Under normal circumstances, the cap "n" collar subfamily of basic region-leucine zipper transcription factor Nrf2 is restricted in the cytoplasm by binding to its ligand Kelch-like ECH associating protein 1 (Keap1). 18 Once exposed to oxidative stress stimulation, Nrf2-Keap1 complexes can be dissociated, the detached Nrf2 translocates into the nucleus to promote hemeoxygenase 1 (HO-1) expression, which involves in the balance of molecules associated with oxidative stress, such as superoxide dismutase (SOD), malonaldehyde (MDA), reactive oxygen species (ROS), and glutathione peroxidase (GSH-Px).…”

Section: Introductionmentioning

confidence: 99%

Loganin Attenuates Septic Acute Renal Injury with the Participation of AKT and Nrf2/HO-1 Signaling Pathways

Zhang¹,

Wang²,

Kang³

et al. 2021

DDDT

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Purpose: Sepsis, a destructive inflammatory response syndrome, is the principal reason to induce death in the intensive care unit. Loganin has been proved to possess the property of anti-inflammation, antioxidant, neuroprotection, and sedation. The primary aim of this study was to evaluate whether Loganin could alleviate acute kidney injury (AKI) during sepsis and investigate the latent mechanisms. Methods: Septic AKI models were established by cecal ligation and puncture (CLP) surgery in mice and given Loganin (20, 40, 80 mg/kg) by gavage. Lipopolysaccharides (LPS)stimulated human kidney proximal tubular (HK2) cells incubated in Loganin (5, 10, 20 μ M) were used to explore the accurate mechanisms. Survival rate, renal function (creatinine and blood urea nitrogen), and renal pathological changes were detected in septic mice. Oxidative stress markers (SOD, GSH-Px, MDA, and SOD), mitochondrial membrane potential, mitochondrial calcium overload, and nuclear factor E2-related factor 2 (Nrf2)/hemeoxygenase 1 (HO-1) pathway activation in vivo and in vitro were determined by commercial kits and Western blot. Cell apoptosis, apoptotic-related protein (cleaved caspase-3, Bcl-2, and Bax) expression and protein kinase B (AKT) phosphorylation in vivo and in vitro were measured by TUNEL staining and Western blot. Finally, AKT blockage by 10 μM LY294002 or Nrf2 inhibition by10 μ M ML385 were utilized to prove the involvement of AKT and Nrf2/HO-1 pathway in AKI during sepsis. Results: We found Loganin treatment (20, 40, 80 mg/kg) mitigated septic AKI reflected by elevated renal function and palliative pathological changes. Oxidative stress and apoptosis in the kidney and LPS-treated HK2 cells were also inhibited by Loganin administration, which was accompanied by AKT and Nrf2/HO-1 pathway activation. Besides, the protective effects of Loganin could be diminished by AKT or Nrf2 blockage, indicating the involvement of AKT and Nrf2/HO-1 pathway. Conclusion: The results suggested that the protective effects of Loganin on AKI during sepsis might be mediated by AKT and Nrf2/HO-1 pathway signaling activation in kidney proximal tubular cells.

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Section: Introductionmentioning

confidence: 99%

Loganin Attenuates Septic Acute Renal Injury with the Participation of AKT and Nrf2/HO-1 Signaling Pathways

Zhang¹,

Wang²,

Kang³

et al. 2021

DDDT

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“…The Keap1/Nrf2/HO-1 signal pathway is closely related to oxidative and anti-oxidative processes [ 24 , 25 ]. Typically, NF-E2-related factor-2 (Nrf2) and Kelch-like ECH associating protein 1 (Keap1) bind together.…”

Section: Introductionmentioning

confidence: 99%

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury by inhibiting alveolar macrophage pyroptosis via the Keap1/Nrf2/HO-1 signaling pathway

et al. 2020

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Background: Lung ischemia-reperfusion injury (LIRI) is a complex pathophysiological process that can lead to poor patient outcomes. Inflammasome-dependent macrophage pyroptosis contributes to organ damage caused by ischemia/reperfusion injury. Oxidative stress and antioxidant enzymes also play an important role in LIRI. In this study, we conducted experiments to investigate whether and how preconditioning with rHMGB1 could ameliorate LIRI in a mouse model. Methods: Adult male BALB/c mice were anesthetized, the left hilus pulmonis was clamped, and reperfusion was performed. rHMGB1 was administered via intraperitoneal injection before anesthesia, and brusatol was given intraperitoneally every other day before surgery. We measured pathohistological lung tissue damage, wet/dry mass ratios of pulmonary tissue, and levels of inflammatory mediators to assess the extent of lung injury. Alveolar macrophage pyroptosis was evaluated by measuring release of lactate dehydrogenase, caspase-1 expression was assessed using flow cytometry, and gasdermin-D expression was analyzed using immunofluorescent staining. Levels of oxidative stress markers and antioxidant enzymes were also analyzed. Results: Preconditioning with rHMGB1 significantly ameliorated lung injury induced by ischemia-reperfusion, based on measurements of morphology, wet/dry mass ratios, as well as expression of IL-1β, IL-6, NF-κB, and HMGB1 in lung tissues. It also alleviated alveolar macrophage pyroptosis, reduced oxidative stress and restored the activity of antioxidant enzymes. These beneficial effects were mediated at least in part by the Keap1/Nrf2/HO-1 pathway, since they were reversed by the pathway inhibitor brusatol. Conclusions: Preconditioning with rHMGB1 may protect against LIRI by suppressing alveolar macrophage pyroptosis. This appears to involve reduction of oxidative stress and promotion of antioxidant enzyme activity via the Keap1/ Nrf2/HO-1 pathway.

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“…Al intoxication treatment is performed with the chelating agent deferoxamine or malic acid [16,17]. Experimental studies have suggested that the use of antioxidants and free radical scavengers such as selenium, melatonin, boric acid, and vitamin C can prevent the deleterious effects of free radicals produced as a result of Al intoxication [18,19]. Plant extracts may ameliorate the toxicosis caused by Al exposure, as they contain several antioxidant molecules [20,21].…”

Section: Introductionmentioning

confidence: 99%

Rhamnus alaternus aqueous extract enhances the capacity of system redox defence and protects hepatocytes against aluminum chloride toxicity in rats

et al. 2021

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Background This study was designed to evaluate the protective effects of a Rhamnus alaternus aqueous extract (RAAE) on aluminum chloride-induced hepatotoxicity in rats. A preliminary phytochemical study and antioxidant activity tests of the extract were performed. Methods A preliminary phytochemical study and antioxidant activity tests of the extract were performed. For the in vivo study, twenty-four male rats were divided into four groups. The control group (C); the RAAE group treated with 250 mg/kg b.w RAAE; the AlCl3 group, which received 50 mg/kg b.w AlCl3; and the AlCl3/RAAE group that was treated with AlCl3 plus RAAE. Results The RAAE contains several phenolic compounds. This plant extract showed a high radical scavenging effect and high antioxidant activity. Administration of AlCl3 resulted in a significant increase in the activities of aspartate aminotransferase and alanine aminotransferase (AST, ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) and significant decreases in the plasma concentrations of total proteins and albumin. Moreover, AlCl3 induced a hepatic pro-oxidant effect leading to an increase in malonaldehyde (MDA) and carbonyl protein contents, the depletion of the content of reduced glutathione (GSH) and a decrease in the antioxidant enzymatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). However, RAAE supplementation with AlCl3 treatment significantly decreased the levels of MDA and carbonyl proteins and markedly restored the activities of the antioxidant enzymes. These results are supported by the improvement in liver tissue restoration. Conclusions The Rhamnus alaternus aqueous extract was shown to have effective antioxidant activity owing to its phenolic compounds protecting against AlCl3-induced liver oxidative damage.

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Selenium-Rich Yeast protects against aluminum-induced peroxidation of lipide and inflammation in mice liver

Cited by 24 publications

References 40 publications

Loganin Attenuates Septic Acute Renal Injury with the Participation of AKT and Nrf2/HO-1 Signaling Pathways

Loganin Attenuates Septic Acute Renal Injury with the Participation of AKT and Nrf2/HO-1 Signaling Pathways

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury by inhibiting alveolar macrophage pyroptosis via the Keap1/Nrf2/HO-1 signaling pathway

Rhamnus alaternus aqueous extract enhances the capacity of system redox defence and protects hepatocytes against aluminum chloride toxicity in rats

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