Effects of apelin and leptin on renal functions following renal ischemia/reperfusion: An experimental study

Sagiroglu, Tamer; Torun, Neşe; Yağcı, Mehmet Ali; Yalta, Tülin; Sagiroglu, Gonul; Oguz, Serhat

doi:10.3892/etm.2012.499

Cited by 32 publications

(31 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…When ischemia persists for a certain duration, following which perfusion recovers, organizational structural and functional recovery may be impaired and kidney dysfunction and structural damage may be aggravated, which is known as IRI (28). Following shock, heart failure, cardiopulmonary bypass or kidney transplantation, IRI usually affects the treatment outcome, particularly in kidney transplant recipients, in which IRI is one of the causes of surgical failure.…”

Section: Discussionmentioning

confidence: 99%

Honokiol protects against renal ischemia/reperfusion injury via the suppression of oxidative stress, iNOS, inflammation and STAT3 in rats

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. Honokiol is the predominant active ingredient in the commonly used traditional Chinese medicine, Magnolia, which has been confirmed in previous studies to exhibit anti-oxidation, antimicrobial, antitumor and other pharmacological effects. However, its effects on renal ischemia/reperfusion injury (IRI) remain to be elucidated. The present study aimed to examine the effects of honokiol on renal IRI, and to investigate its potential protective mechanisms in the heart. Male adult Wistar albino rats were induced into a renal IRI model. Subsequently, the levels of serum creatinine, blood urea nitrogen (BUN), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), and the levels of serum nitrite and the kidney nitrite were examined in the IRI group. The levels of oxidative stress, inducible nitric oxide synthase (iNOS), inflammatory factors and caspase-3 were evaluated using a series of commercially available kits. The levels of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) and the protein expression levels of STAT3 were determined using western blotting. Pretreatment with honokiol significantly reduced the levels of serum creatinine, BUN, ALT, AST and ALP, and the level of nitrite in the kidney of the IRI group, compared with the control group. The levels of malondialdehyde, the activity of myeloperoxidase, and the gene expression and activity of iNOS were reduced in the IRI rats, compared with the sham-operated rats, whereas the levels of superoxide dismutase and catalase were increased following treatment with honokiol in the IRI rats. In addition, the expression levels of tumor necrosis factor-α and interleukin-6 in the IRI rats were increased by honokiol. Treatment with honokiol suppressed the protein expression levels of p-STAT3 and caspase-3 in the IRI rats. These findings indicated that honokiol protects against renal IRI via the suppression of oxidative stress, iNOS, inflammation and STAT3 in the rat.

show abstract

Section: Discussionmentioning

confidence: 99%

Honokiol protects against renal ischemia/reperfusion injury via the suppression of oxidative stress, iNOS, inflammation and STAT3 in rats

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…46 Renal I/R injury usually causes primary tubular epithelial cell injury, in-47 cluding tubular obstruction and reduced tubular re-absorption of NaCl. 48 However, several studies reported that hemodynamic changes induced 49 by renal I/R injury also occur, which lead to mesangial contraction and 50 cessation of glomerular filtration. Thus, the interaction of microvascular 51 (including glomerular and medullary parts) and tubular events both 52 contribute to the pathogenesis of acute ischemic renal failure [4,5].…”

mentioning

confidence: 97%

Apelin protects against acute renal injury by inhibiting TGF-β1

Chen

Wan

Wang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Renal ischemia/reperfusion (I/R) injury is the most common cause of acute kidney injury, having a high rate of mortality and no effective therapy currently available. Apelin-13, a bioactive peptide, has been shown to inhibit the early lesions of diabetic nephropathy in several mouse models by us and others. To test whether apelin-13 protects against renal I/R induced injury, male rats were exposed to renal I/R injury with or without apelin-13 treatment for 3 days. Apelin-13 treatment markedly reduced the injury-induced tubular lesions, renal cell apoptosis, and normalized the injury induced renal dysfunction. Apelin-13 treatment inhibited the injury-induced elevation of inflammatory factors and Tgf-β1, as well as apoptosis. Apelin-13 treatment also inhibited the injury-induced elevation of histone methylation and Kmt2d, a histone methyltransferase of H3K4me2, following renal I/R injury. Furthermore, in cultured renal mesangial and tubular cells, apelin-13 suppressed the injury-induced elevation of Tgf-β1, apoptosis, H3K4me2 and Kmt2d under the in vitro hypoxia/reperfusion (H/R) conditions. Consistently, over-expression of apelin significantly inhibited H/R-induced elevation of TGF-β1, apoptosis, H3K4me2 and Kmt2d. The present study therefore suggests apelin-13 may be a therapeutic candidate for treating acute kidney injury.

show abstract

“…Apelins and APJ are widely expressed in animal and human heart, lung, kidney, brain, liver, breast, and skeletal muscle and abundantly found in cardiovascular, brain, lung, and breast cancers. Previous studies have shown that apelin/APJ system has effects on the function of cardiovascular system [4], has the functional and histopathological protective effects against renal ischemia/ reperfusion injury [5], and has the effect of analgesia [6]. In addition, apelin/APJ system is involved in many processes such as regulation of the release of hormone and metabolism [7], regulation of cell proliferation, migration, and apoptosis [8], and reduction of pulmonary inflammation and fibrin deposition [9].…”

Section: Introductionmentioning

confidence: 99%

ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13

Yang

et al. 2014

ABBS

View full text Add to dashboard Cite

The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcinoma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B (LC3A/B), and beclin1, and confirmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. Moreover, there are pores on the surface of human lung adenocarcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force microscopy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation.

show abstract

Effects of apelin and leptin on renal functions following renal ischemia/reperfusion: An experimental study

Cited by 32 publications

References 26 publications

Honokiol protects against renal ischemia/reperfusion injury via the suppression of oxidative stress, iNOS, inflammation and STAT3 in rats

Honokiol protects against renal ischemia/reperfusion injury via the suppression of oxidative stress, iNOS, inflammation and STAT3 in rats

Apelin protects against acute renal injury by inhibiting TGF-β1

ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13

Contact Info

Product

Resources

About