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DMF attenuates cisplatin-induced kidney injury via activating Nrf2 signaling pathway and inhibiting NF-kB signaling pathway.
Eur Rev Med Pharmacol Sci. 2018 12; 22(24):8924-8931.ER

Abstract

OBJECTIVE

N,N-dimethylformamide (DMF) exerts anti-inflammatory and anti-oxidant capacities. We aim to explore whether DMF could regulate cisplatin-induced kidney injury in rats via NF-E2-related factor 2 (Nrf2) pathway and nuclear factor-κB (NF-κB) pathway.

MATERIALS AND METHODS

A total of 30 Sprague Dawley (SD) rats were randomly assigned into sham group, cisplatin treatment group (DDP group) and DMF + cisplatin treatment group (DMF group), with 10 rats in each group. After 10 days of treatment, we collected serum and kidney samples of rats. Serum levels of creatinine (Cr) and urea nitrogen (BUN) were detected using relative commercial kits. Hematoxylin-eosin (HE) staining was performed to observe pathological changes of kidneys. The relevant oxidative stress indicators in the kidney homogenates of each group were detected by commercial kits, including malondialdehyde (MDA), total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) and monoamine oxidase (MAO). Protein expressions of Nrf2 and NF-κB in kidney tissues were detected by Western blot.

RESULTS

Serum levels of Cr and BUN were lower in DMF group than those of DDP group. Higher activities of SOD, GSH, CAT and T-AOC were found in DMF group compared with those of DDP group. However, MAD and ROS contents were remarkably decreased in DMF group than those of DDP group. DMF pretreatment remarkably reduced renal pathological changes. Western blot analysis also indicated that DMF effectively upregulated expression levels of Nrf2, Heme Oxygenase-1 (HO-1) and NAD (P) H, quinine oxidoreductase 1 (NQO-1), while downregulated NF-κB.

CONCLUSIONS

DMF could inhibit oxidative stress by activating Nrf2 signaling pathway and reduce inflammatory response by attenuating NF-κB signaling pathway, thus protecting cisplatin-induced kidney injury.

Authors+Show Affiliations

Department of Physiology, Qiqihar Medical University, Qiqihar, China. 514070919@qq.com.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30575936

Citation

Zhao, K, and L-B Wen. "DMF Attenuates Cisplatin-induced Kidney Injury Via Activating Nrf2 Signaling Pathway and Inhibiting NF-kB Signaling Pathway." European Review for Medical and Pharmacological Sciences, vol. 22, no. 24, 2018, pp. 8924-8931.
Zhao K, Wen LB. DMF attenuates cisplatin-induced kidney injury via activating Nrf2 signaling pathway and inhibiting NF-kB signaling pathway. Eur Rev Med Pharmacol Sci. 2018;22(24):8924-8931.
Zhao, K., & Wen, L. B. (2018). DMF attenuates cisplatin-induced kidney injury via activating Nrf2 signaling pathway and inhibiting NF-kB signaling pathway. European Review for Medical and Pharmacological Sciences, 22(24), 8924-8931. https://doi.org/10.26355/eurrev_201812_16662
Zhao K, Wen LB. DMF Attenuates Cisplatin-induced Kidney Injury Via Activating Nrf2 Signaling Pathway and Inhibiting NF-kB Signaling Pathway. Eur Rev Med Pharmacol Sci. 2018;22(24):8924-8931. PubMed PMID: 30575936.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - DMF attenuates cisplatin-induced kidney injury via activating Nrf2 signaling pathway and inhibiting NF-kB signaling pathway. AU - Zhao,K, AU - Wen,L-B, PY - 2018/12/22/entrez PY - 2018/12/24/pubmed PY - 2020/1/14/medline SP - 8924 EP - 8931 JF - European review for medical and pharmacological sciences JO - Eur Rev Med Pharmacol Sci VL - 22 IS - 24 N2 - OBJECTIVE: N,N-dimethylformamide (DMF) exerts anti-inflammatory and anti-oxidant capacities. We aim to explore whether DMF could regulate cisplatin-induced kidney injury in rats via NF-E2-related factor 2 (Nrf2) pathway and nuclear factor-κB (NF-κB) pathway. MATERIALS AND METHODS: A total of 30 Sprague Dawley (SD) rats were randomly assigned into sham group, cisplatin treatment group (DDP group) and DMF + cisplatin treatment group (DMF group), with 10 rats in each group. After 10 days of treatment, we collected serum and kidney samples of rats. Serum levels of creatinine (Cr) and urea nitrogen (BUN) were detected using relative commercial kits. Hematoxylin-eosin (HE) staining was performed to observe pathological changes of kidneys. The relevant oxidative stress indicators in the kidney homogenates of each group were detected by commercial kits, including malondialdehyde (MDA), total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) and monoamine oxidase (MAO). Protein expressions of Nrf2 and NF-κB in kidney tissues were detected by Western blot. RESULTS: Serum levels of Cr and BUN were lower in DMF group than those of DDP group. Higher activities of SOD, GSH, CAT and T-AOC were found in DMF group compared with those of DDP group. However, MAD and ROS contents were remarkably decreased in DMF group than those of DDP group. DMF pretreatment remarkably reduced renal pathological changes. Western blot analysis also indicated that DMF effectively upregulated expression levels of Nrf2, Heme Oxygenase-1 (HO-1) and NAD (P) H, quinine oxidoreductase 1 (NQO-1), while downregulated NF-κB. CONCLUSIONS: DMF could inhibit oxidative stress by activating Nrf2 signaling pathway and reduce inflammatory response by attenuating NF-κB signaling pathway, thus protecting cisplatin-induced kidney injury. SN - 2284-0729 UR - https://www.unboundmedicine.com/medline/citation/30575936/DMF_attenuates_cisplatin_induced_kidney_injury_via_activating_Nrf2_signaling_pathway_and_inhibiting_NF_kB_signaling_pathway_ L2 - https://www.europeanreview.org/article/16662 DB - PRIME DP - Unbound Medicine ER -