Renoprotective effect of yohimbine on ischaemia/reperfusion-induced acute kidney injury through α2C-adrenoceptors in rats

Shimokawa, Takaomi; Tsutsui, Hidenobu; Miura, Takeshi; Nishinaka, Toru; Terada, Tomoyuki; Takama, Masashi; Yoshida, Shuhei; Tanba, Takao; Tojo, Ayumi; Yamagata, Masayo; Yukimura, Tokihito

doi:10.1016/j.ejphar.2016.03.059

Cited by 16 publications

(13 citation statements)

References 35 publications

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“…However, the exact molecular mechanisms underlying renal I/R injury are not completely understood. Various pharmaceuticals have been identified for the treatment of renal I/R injury in the laboratory, such as AICAR (5-amino-4-imidazolecarboxamide riboside-1-b-D-ribofuranoside), yohimbine, and pioglitazone [4,5,6]. However, these are limited, and few renal protectants have been successfully translated into clinical applications.…”

Section: Introductionmentioning

confidence: 99%

Genistein Ameliorates Ischemia/Reperfusion-Induced Renal Injury in a SIRT1-Dependent Manner

Yang

Zhu

et al. 2017

Nutrients

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Renal ischemia/reperfusion (I/R) injury continues to be a complicated situation in clinical practice. Genistein, the main isoflavone found in soy products, is known to possess a wide spectrum of biochemical and pharmacological activities. However, the protective effect of genistein on renal I/R injury has not been well investigated. In the current study, we explore whether genistein exhibits its renal-protective effects through SIRT1 (Sirtuin 1) in I/R-induced mice model. We found the treatment of genistein significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Meanwhile, SIRT1 expression was up-regulated following the administration of genistein in renal region. Furthermore, pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the protective effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury, suggesting an indispensible role of the increased SIRT1 expression and activity in this process. Meanwhile, the reduced p53 and p21 expression and increased PCNA (Proliferating Cell Nuclear Antigen) expression were blocked after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process. Hence, our results provided further experimental basis for the potential use of genistein for the treatment of kidney disease with deficiency of SIRT1 activity.

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Section: Introductionmentioning

confidence: 99%

Genistein Ameliorates Ischemia/Reperfusion-Induced Renal Injury in a SIRT1-Dependent Manner

Yang

Zhu

et al. 2017

Nutrients

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“…31,46 The α 2 -adrenoceptor-dependent renal pro-inflammatory effects include activation of pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) as well as increased granulocyte and monocyte recruitment. Studies in rats uninephrectomized before IR and mice that underwent unilateral IR have shown that systemic α 2 -adrenoceptor blockade (non-selective α 2 -adreoceptor blockers yohimbine and atipamezole, α 2c -adroceptor blocker JP-1302) preceding both clamp-induced ischaemia and intra-renal noradrenaline administration reduced tubular damage.…”

Section: Griskmentioning

confidence: 99%

“…31,[44][45][46] Analysis of potential reasons for this is complicated since respective studies differ with regard to the species, type of IR and anaesthetics used during IR. 31,[44][45][46] Analysis of potential reasons for this is complicated since respective studies differ with regard to the species, type of IR and anaesthetics used during IR.…”

Section: Sns Activationmentioning

confidence: 99%

“…10 During acute renal ischaemia, the activity of renal sensory nerves was found to be elevated. 25,26,36 Visceral spinal afferent neurons including nociceptors can be activated by substances released from damaged tissues (so called damage or danger-associated molecular patterns, DAMPs); 8 Unilateral after UNX 1 44 Unilateral without UNX 1 31 Rat Bilateral 2 45,54 Unilateral after UNX 13 20,[23][24][25]27,28,[33][34][35]46,50,69,73 Unilateral without UNX 3 26,39,52 Rabbit Unilateral after UNX 2 42,43 Dog Unilateral after UNX 1 49 Abbreviation: UNX, uninephrectomy.…”

Section: In Experimental Renal Irmentioning

confidence: 99%

“…Many studies reported beneficial effects of sympathetic inhibition on renal structure and excretory function in experimental IR performed in rabbits, rats and mice. These interventions include generalized SNS inhibition by centrally acting sympatholytic agents administered intravenously (iv), intraperitoneally (ip) or ICV, 24,[33][34][35][42][43][44][45] ganglionic blockade, 23 α 2 -adrenoceptor blockade, 31,46 non-selective β-adrenoceptor blockade, 47 chemical sympathectomy 29 and local renal denervation prior to or immediately after IR. 23,30,31,48 In dogs, administration of a β 1 -adrenoceptor blocker was without beneficial effects in this setting.…”

Section: Mitigates Experimental Ir-induced Renal Injurymentioning

confidence: 99%

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The sympathetic nervous system in acute kidney injury

Grisk

2019

Acta Physiologica

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Acute kidney injury (AKI) is frequently accompanied by activation of the sympathetic nervous system (SNS). This may result from pre-exisiting chronic diseases associated with sympathetic activation prior to AKI or it may be induced by stressors that ultimately lead to AKI such as endotoxins and arterial hypotension in circulatory shock. Conversely, sympathetic activation may also result from acute renal injury. Focusing on studies in experimental renal ischaemia and reperfusion (IR), this review summarizes the current knowledge on how the SNS is activated in IR-induced AKI and on the consequences of sympathetic activation for the development of acute renal damage. Experimental studies show beneficial effects of sympathoinhibitory interventions on renal structure and function in response to IR. However, few clinical trials obtained in scenarios that correspond to experimental IR, namely major elective surgery, showed that peri-operative treatment with centrally acting sympatholytics reduced the incidence of AKI. Apparently, discrepant findings on how sympathetic activation influences renal responses to acute IR-induced injury are discussed and future areas of research in this field are identified.

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