Therapeutic effects of CORM3 and NaHS in chronic kidney disease induced cognitive impairment via the interaction between carbon monoxide and hydrogen sulfide on Nrf2/HO-1 signaling pathway in rats

硫化氢钠 血红素加氧酶 海马体 内科学 肾脏疾病 锌原卟啉 医学 化学 内分泌学 硫化氢 血红素 生物化学 有机化学 硫黄
作者
Zeinab Hamidizad,Mehri Kadkhodaee,Seyed Morteza Karimian,Mina Ranjbaran,Fatemeh Heidari,Enayatollah Bakhshi,Farzaneh Kianian,Elham Zahedi,Behjat Seifi
出处
期刊:Chemico-Biological Interactions [Elsevier BV]
卷期号:368: 110217-110217 被引量:10
标识
DOI:10.1016/j.cbi.2022.110217
摘要

Cognitive impairment is one of the major complications of chronic kidney disease (CKD). The present study aims to evaluate the protective effects of carbon monoxide (CO) and hydrogen sulfide (H2S) and their interactions on CKD-induced cognitive deficits by considering the Nrf2/HO-1 signaling pathway. Sixty rats were divided into six experimental groups: sham, five-sixth (5/6) nephrectomy (CKD), CKD + H2S donor (NaHS), CKD + CO-releasing molecule (CORM3), CKD + NaHS and zinc protoporphyrin IX (Znpp), CKD + CORM3 and amino-oxy acetic acid (AOAA). Eleven weeks after 5/6Nx, behavioral tests (Novel object recognition test, Passive avoidance test and Barnes maze test) were performed to evaluate the cognitive level. At the end of the twelfth week, blood urea nitrogen (BUN) and serum creatinine (sCr) levels, as well as the expression levels of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), and neuronal loss in the hippocampus and prefrontal cortex were evaluated. CKD caused enhancement of BUN and sCr, reduction of Nrf2 and HO-1 proteins and enhancement of neuronal loss in the hippocampus and prefrontal cortex. In addition, CKD led to cognitive disturbances and memory impairment. CORM3 and NaHS returned all above indices to the levels measured in the control group. However, improving effects of CORM3 on cognitive impairment and Nrf2/HO-1 signaling pathway were prevented by AOAA and decreased H2S level as well as reciprocally improving effects of NaHS on cognitive disturbances and Nrf2/HO-1 signaling pathway were prevented by Znpp and decreased CO level. In conclusion, this study demonstrated that formation of CO and H2S were interdependently improved CKD-induced cognitive dysfunctions, through interaction with Nrf2/HO-1 signaling pathway.
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