Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway
The major component of the <i>Solenocera crassicornis</i> 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. I...
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MDPI AG
2020-08-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/9/8/745 |
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| author | Shuoqi Jiang Zhuangwei Zhang FangFang Huang Zuisu Yang Fangmiao Yu Yunping Tang Guofang Ding |
| author_facet | Shuoqi Jiang Zhuangwei Zhang FangFang Huang Zuisu Yang Fangmiao Yu Yunping Tang Guofang Ding |
| author_sort | Shuoqi Jiang |
| collection | DOAJ |
| description | The major component of the <i>Solenocera crassicornis</i> 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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| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T17:30:06Z |
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| spelling | doaj.art-deccb13a0d2646e5bad389eec94506a02023-11-20T10:03:57ZengMDPI AGAntioxidants2076-39212020-08-019874510.3390/antiox9080745Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 PathwayShuoqi Jiang0Zhuangwei Zhang1FangFang Huang2Zuisu Yang3Fangmiao Yu4Yunping Tang5Guofang Ding6Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaZhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, ChinaThe major component of the <i>Solenocera crassicornis</i> 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.https://www.mdpi.com/2076-3921/9/8/745apoptosiscyclophosphamideinflammationoxidative stresspeptides<i>Solenocera crassicornis</i> |
| spellingShingle | Shuoqi Jiang Zhuangwei Zhang FangFang Huang Zuisu Yang Fangmiao Yu Yunping Tang Guofang Ding Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway Antioxidants apoptosis cyclophosphamide inflammation oxidative stress peptides <i>Solenocera crassicornis</i> |
| title | Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway |
| title_full | Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway |
| title_fullStr | Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway |
| title_full_unstemmed | Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway |
| title_short | Protective Effect of Low Molecular Weight Peptides from <i>Solenocera crassicornis</i> Head against Cyclophosphamide-Induced Nephrotoxicity in Mice <i>via</i> the Keap1/Nrf2 Pathway |
| title_sort | protective effect of low molecular weight peptides from i solenocera crassicornis i head against cyclophosphamide induced nephrotoxicity in mice i via i the keap1 nrf2 pathway |
| topic | apoptosis cyclophosphamide inflammation oxidative stress peptides <i>Solenocera crassicornis</i> |
| url | https://www.mdpi.com/2076-3921/9/8/745 |
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