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C-type natriuretic peptide ameliorates ischemia/reperfusion-induced acute kidney injury by inhibiting apoptosis and oxidative stress in rats.
Life Sci. 2014 Nov 04; 117(1):40-5.LS

Abstract

AIMS

Although atrial natriuretic peptide has been shown to attenuate ischemia-reperfusion (IR)-induced kidney injury, the effect of natriuretic peptide receptor (NPR)-B activation on IR-induced acute kidney injury is not well documented. The purpose of the present study was to identify the effect of C-type natriuretic peptide (CNP), a selective activator of NPR-B, on the IR-induced acute kidney injury and its mechanisms involved.

MAIN METHODS

Unilaterally nephrectomized rats were insulted by IR in their remnant kidney, and they were randomly divided into three groups: sham, vehicle+IR, and CNP+IR groups. CNP (0.2μg/kg/min) was administered intravenously at the start of a 45-min renal ischemia for 2h. Rats were then killed 24h after I/R, and the blood and tissue samples were collected to assess renal function, histology, TUNEL assay, and Western blot analysis of kidney Bax and Bcl-2 expressions.

KEY FINDINGS

The levels of blood urea nitrogen and serum creatinine were significantly increased in rats after IR compared with vehicle-treated rats. IR elevated apoptosis, Bcl-2/Bax ratio, TUNEL positivity, oxidative stress parameters, malondialdehyde concentration, and superoxide dismutase activity. IR also induced epithelial desquamation of the proximal tubules and glomerular shrinkage. CNP significantly attenuated the IR-induced increase in BUN and serum creatinine. Furthermore, CNP restored the suppressed renal cyclic guanosine 3' 5'-monophosphate levels caused by IR insult.

SIGNIFICANCE

Study findings suggest that CNP could ameliorate IR-induced acute kidney injury through inhibition of apoptotic and oxidative stress pathways, possibly through NPR-B-cGMP signaling.

Authors+Show Affiliations

Department of Urology, Affiliated Hospital of Yanbian University, Yanji (133000), Jilin Province, China.Department of Anatomy, Medical College of Yanbian University, Yanji (133000), Jilin Province, China.Department of Anatomy, Medical College of Yanbian University, Yanji (133000), Jilin Province, China.Department of Anatomy, Medical College of Yanbian University, Yanji (133000), Jilin Province, China.Department of Anatomy, Medical College of Yanbian University, Yanji (133000), Jilin Province, China. Electronic address: dyxu@ybu.edu.cn.

Pub Type(s)

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

Language

eng

PubMed ID

25283078

Citation

Jin, Xiunan, et al. "C-type Natriuretic Peptide Ameliorates Ischemia/reperfusion-induced Acute Kidney Injury By Inhibiting Apoptosis and Oxidative Stress in Rats." Life Sciences, vol. 117, no. 1, 2014, pp. 40-5.
Jin X, Zhang Y, Li X, et al. C-type natriuretic peptide ameliorates ischemia/reperfusion-induced acute kidney injury by inhibiting apoptosis and oxidative stress in rats. Life Sci. 2014;117(1):40-5.
Jin, X., Zhang, Y., Li, X., Zhang, J., & Xu, D. (2014). C-type natriuretic peptide ameliorates ischemia/reperfusion-induced acute kidney injury by inhibiting apoptosis and oxidative stress in rats. Life Sciences, 117(1), 40-5. https://doi.org/10.1016/j.lfs.2014.09.023
Jin X, et al. C-type Natriuretic Peptide Ameliorates Ischemia/reperfusion-induced Acute Kidney Injury By Inhibiting Apoptosis and Oxidative Stress in Rats. Life Sci. 2014 Nov 4;117(1):40-5. PubMed PMID: 25283078.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - C-type natriuretic peptide ameliorates ischemia/reperfusion-induced acute kidney injury by inhibiting apoptosis and oxidative stress in rats. AU - Jin,Xiunan, AU - Zhang,Youchen, AU - Li,Xiangdan, AU - Zhang,Jun, AU - Xu,Dongyuan, Y1 - 2014/10/02/ PY - 2014/04/10/received PY - 2014/08/30/revised PY - 2014/09/20/accepted PY - 2014/10/7/entrez PY - 2014/10/7/pubmed PY - 2015/1/30/medline KW - Acute kidney injury KW - Apoptotic change KW - C-type natriuretic peptide (PubChem CID: 16179407) KW - CNP KW - Oxidative stress KW - cGMP SP - 40 EP - 5 JF - Life sciences JO - Life Sci VL - 117 IS - 1 N2 - AIMS: Although atrial natriuretic peptide has been shown to attenuate ischemia-reperfusion (IR)-induced kidney injury, the effect of natriuretic peptide receptor (NPR)-B activation on IR-induced acute kidney injury is not well documented. The purpose of the present study was to identify the effect of C-type natriuretic peptide (CNP), a selective activator of NPR-B, on the IR-induced acute kidney injury and its mechanisms involved. MAIN METHODS: Unilaterally nephrectomized rats were insulted by IR in their remnant kidney, and they were randomly divided into three groups: sham, vehicle+IR, and CNP+IR groups. CNP (0.2μg/kg/min) was administered intravenously at the start of a 45-min renal ischemia for 2h. Rats were then killed 24h after I/R, and the blood and tissue samples were collected to assess renal function, histology, TUNEL assay, and Western blot analysis of kidney Bax and Bcl-2 expressions. KEY FINDINGS: The levels of blood urea nitrogen and serum creatinine were significantly increased in rats after IR compared with vehicle-treated rats. IR elevated apoptosis, Bcl-2/Bax ratio, TUNEL positivity, oxidative stress parameters, malondialdehyde concentration, and superoxide dismutase activity. IR also induced epithelial desquamation of the proximal tubules and glomerular shrinkage. CNP significantly attenuated the IR-induced increase in BUN and serum creatinine. Furthermore, CNP restored the suppressed renal cyclic guanosine 3' 5'-monophosphate levels caused by IR insult. SIGNIFICANCE: Study findings suggest that CNP could ameliorate IR-induced acute kidney injury through inhibition of apoptotic and oxidative stress pathways, possibly through NPR-B-cGMP signaling. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/25283078/C_type_natriuretic_peptide_ameliorates_ischemia/reperfusion_induced_acute_kidney_injury_by_inhibiting_apoptosis_and_oxidative_stress_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(14)00796-6 DB - PRIME DP - Unbound Medicine ER -