The Ameliorating Effect of Plasma Protein from Tachypleus tridentatus on Cyclophosphamide-Induced Acute Kidney Injury in Mice

Jing, Mengyao; Zhang, Guoguang; He, Lanzheng; Hong, Pengzhi; Deng, Chunmei

doi:10.3390/md17040227

Cited by 22 publications

(25 citation statements)

References 19 publications

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“…As mentioned, SCHPs-F1 increased the antioxidant defense parameters GSH-Px, SOD, CAT, and T-AOC and decreased levels of the lipid peroxidation marker MDA, thereby potentially alleviating oxidative stress of CTX-exposed kidneys. A similar mechanism to enhance the endogenous antioxidant defense to alleviate CTX-induced renal injury was reported for aminoguanidine [35], Olea europaea leaf extract [6], and plasma protein from Tachypleus tridentatu [21].…”

Section: Discussionsupporting

confidence: 63%

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Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

et al. 2020

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The major component of the Solenocera crassicornis head protein hydrolysates-fraction 1 (SCHPs-F1) are low molecular weight peptides (MW < 1 kDa). In this study, we investigated the potential renoprotective effects of SCHPs-F1 in a cyclophosphamide (CTX) toxicity mouse model. In brief, 40 male mice were randomly divided into 5 groups and received either saline or 80 mg/kg body weight (BW) CTX by intraperitoneal injection for 5 days, followed by either saline or SCHPs-F1 (100, 200, and 400 mg/kg BW) by intragastric administration for 15 days. SCHPs-F1 treatment significantly reversed the CTX-induced decreases in the levels of blood urea nitrogen (BUN), creatinine (CRE), and cytochrome P450 (CYP450), as well as the renal histological lesions. Furthermore, the results indicated that SCHPs-F1 potentially alleviated CTX-induced nephrotoxicity through mitigating inflammatory responses, oxidative stress, and apoptosis status of the kidneys, as evidenced by decreased levels of malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ and increased levels of total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Moreover, overexpression of pro-apoptotic proteins pair B-cell lymphoma-2 (Bcl-2)-associated X (Bax)/Bcl-2, cysteinyl aspartate specific proteinase (caspase)-3 and caspase-9 in renal tissues were suppressed by treatment with SCHPs-F1. In addition, the protein levels of the antioxidant factor nuclear factor erythroid-2 related factor 2 (Nrf2) and the expression levels of its downstream target genes heme-oxygenase (HO-1), glutamate-cysteine ligase modifier subunit (GCLM) and NAD(P)H dehydrogenase (quinone) 1 (NQO-1) were stimulated by treatment with SCHPs-F1 in the CTX-induced renal injury model. Taken together, our data suggested that SCHPs-F1 could provide a novel potential strategy in mitigating the nephrotoxicity caused by CTX.

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Section: Discussionsupporting

confidence: 63%

“…The kidneys are important metabolic organs in mammals; they excrete metabolic waste and chemical metabolites by filtering urine and maintain homeostasis and normal physiological activities [21]. Several studies have shown that the nephrotoxicity of CTX metabolites is a serious limitation in cancer chemotherapy [9,22].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

et al. 2020

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“…Oxidative Medicine and Cellular Longevity induced AKI through effective prevention of apoptosis in CDDP-exposed renal tissues as previously mentioned in cyclophosphamide-induced AKI [71]. Moreover, to further elucidate the proved complex interaction between autophagy and apoptosis in CDDP-induced nephrotoxicity [72], we noticed that the expressions of key apoptotic caspases, caspase-3, as well as TDT, were inhibited and accompanied by downregulation in autophagy-related protein, LC3 II, indicating that the occurrence of apoptosis may be regulated by autophagy.…”

mentioning

confidence: 77%

“…Furthermore, we suggested that CDDP caused excessive ROS production (high H 2 O 2 levels) where antioxidants such as SOD would be consumed destroying the bal-ance between ROS and antioxidant systems leading to autophagy-mediated apoptosis. Kang et al [71] have documented that the combined action of oxidative stress imbalance and autophagy defects causes abnormal cell apoptosis which leads to the occurrence of AKI [71]. Indeed, it is undeniable that the disruption of growth factors and their receptors play a role in CDDP-induced renal injuries [56].…”

mentioning

confidence: 99%

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

Mahran

Hassan

2020

Oxidative Medicine and Cellular Longevity

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Background. Cisplatin (cis-diaminedichloroplatinum, CDDP) is a broad-spectrum antineoplastic agent. However, CDDP has been blamed for its nephrotoxicity, which is the main dose-limiting adverse effect. Ganoderma lucidum (GL), a medicinal mushroom, has antioxidant and inflammatory activities. Therefore, this study is aimed at finding out the potential nephroprotection of GL against CDDP-induced nephrotoxicity in rats and the possible molecular mechanisms including the EGFR downstream signaling, apoptosis, and autophagy. Methods. Rats were given GL (500 mg/kg) for 10 days and a single injection of CDDP (12 mg/kg, i.p). Results. Nephrotoxicity was evidenced by a significant increase in renal indices and oxidative stress markers. Additionally, CDDP showed a plethora of inflammatory and apoptotic responses as evidenced by a profound increase of HMGB-1, NF-κB, and caspase-3 expressions, whereas administration of GL significantly improved all these indices as well as the histopathological insults. Renal expression of EGFR showed a similar trend after GL administration. Furthermore, activation of autophagy protein, LC3 II, was found to be involved in GL-mediated nephroprotection correlated with the downregulation of apoptotic signaling, caspase-3 and terminal deoxynucleotidyl transferase (TDT) renal expressions. Conclusion. These results suggest that GL might have improved CDDP-induced nephrotoxicity through antioxidant, anti-inflammatory, and autophagy-mediated apoptosis mechanisms and that inhibition of EGFR signaling might be involved in nephroprotection.

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“…P38MAPK phosphorylation is essentially responsible for the production of the C-C chemokine, monocyte chemoattractant protein (MCP)-1, which is involved in the pathogenesis of LN [27]. Further studies have shown that the p38MAPK signalling pathway plays a crucial role in the transcription and translation of different components of the p38MAPK signalling pathway before the pro-in ammatory cytokine synthesis, constituting potential therapeutic targets for in ammatory diseases and autoimmune diseases [28][29][30]. Therefore, the present study focused on the p38MAPK signalling pathway, which has been implicated in LN progression, because it exerts important immune regulatory functions and regulates cell apoptosis and in ammatory responses [31][32][33].…”

Section: Introductionmentioning

confidence: 99%

Depletion of Fractalkine Ameliorates Renal Injury and Treg Cell Apoptosis Via the p38MAPK Pathway in Lupus-prone Mice

Gong

Guo

et al. 2020

Preprint

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Background: Fractalkine is a chemokine with several roles, including chemotaxis, adhesion, and immune damage. It participates in cell inflammation and apoptosis and responds to the pathogenesis of autoimmune diseases. On the other hand, Treg cells are involved in autoimmune diseases. This study aimed to explore the regulatory mechanism of Fractalkine in renal injury and Treg apoptosis via the p38MAPK signalling pathway in lupus-prone mice. Methods: Lupus was induced in BALB/c female mice by injection of pristane. Then, CD4+ CD5+ Treg cells were isolated from the spleen of lupus mice. To deplete Fractalkine, first, mice received an injection of anti-Fractalkine antibody. Later, the transfection of Treg cells with Fractalkine siRNA was conducted. Lupus mice and Treg cells were treated with the p38MAPK inhibitor SB203580 and/or activator U-46619, respectively. The levels of urine protein, serum urea nitrogen, creatinine, and autoantibodies were measured from mouse samples, and renal histopathological features were analysed. The expression of Fractalkine, p-p38, Foxp3, IL-6, and IL-17 in the mouse kidney and Treg cells was detected. The levels of apoptosis and key apoptotic factors: Bax, Bcl-2, and Cyt-c in Treg cells were analysed. Results: The expression of Fractalkine, p-p38, IL-6, and IL-17 increased; meanwhile, that of Foxp3 decreased in the kidneys of mice with lupus. The depletion of Fractalkine and p38MAPK levels ameliorated proteinuria and renal functions and significantly reduced serum autoantibodies, renal Fractalkine, p-p38, IL-6, and IL-17 levels, while increasing renal Foxp3 concentration in lupus mice. The effects of Fractalkine knockdown (KD) and p38MAPK inhibitor on Treg cells, derived from lupus mice, were consistent with those observed in the kidneys. In addition, Fractalkine KD reduced cell apoptosis and suppressed the activation of p38MAPK signalling in Treg cells, derived from lupus mice. Meanwhile, the p38MAPK activator U-46619 had the opposite effect. Conclusion: Together, our data indicated that Fractalkine promoted the nephritis progression in lupus mice, most likely through the regulation of Treg cell apoptosis and activation of the p38MAPK signalling pathway. It suggested that targeting Fractalkine is a potential therapeutic strategy for treating LN.

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The Ameliorating Effect of Plasma Protein from Tachypleus tridentatus on Cyclophosphamide-Induced Acute Kidney Injury in Mice

Cited by 22 publications

References 19 publications

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

Depletion of Fractalkine Ameliorates Renal Injury and Treg Cell Apoptosis Via the p38MAPK Pathway in Lupus-prone Mice

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