Hypothermia induced by adenosine 5′‐monophosphate attenuates injury in an <scp>L</scp>‐arginine‐induced acute pancreatitis rat model

Wang, Yunlong; Guo, Weiting; Li, Yuan; Pan, Xinting; Lv, Wenshan; Cui, Lingling; Li, Changgui; Wang, Yangang; Yan, Shushan; Zhang, Jidong; Liu, Bin

doi:10.1111/jgh.12448

Cited by 12 publications

(11 citation statements)

References 25 publications

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“…Large exogenous doses of AMP (500 to 3500 mg/kg) cause torpor and have protective effects in various injury models (Miao et al , 2015; Miao et al , 2012; Tao et al , 2011; Wang et al , 2014). There is no clearly identified receptor for AMP (although AMP has been proposed to be an A 1 AR ligand (Rittiner et al , 2012)).…”

Section: Discussionmentioning

confidence: 99%

Hypothermia in mouse is caused by adenosine A1 and A3 receptor agonists and AMP via three distinct mechanisms

et al. 2017

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Small mammals have the ability to enter torpor, a hypothermic, hypometabolic state, allowing impressive energy conservation. Administration of adenosine or adenosine 5'-monophosphate (AMP) can trigger a hypothermic, torpor-like state. We investigated the mechanisms for hypothermia using telemetric monitoring of body temperature in wild type and receptor knock out (Adora1−/−, Adora3−/−) mice. Confirming prior data, stimulation of the A3 adenosine receptor (AR) induced hypothermia via peripheral mast cell degranulation, histamine release, and activation of central histamine H1 receptors. In contrast, A1AR agonists and AMP both acted centrally to cause hypothermia. Commonly used, selective A1AR agonists, including N6-cyclopentyladenosine (CPA), N6-cyclohexyladenosine (CHA), and MRS5474, caused hypothermia via both A1AR and A3AR when given intraperitoneally. Intracerebroventricular dosing, low peripheral doses of Cl-ENBA [(±)-5'-chloro-5'-deoxy-N6-endo-norbornyladenosine], or using Adora3−/− mice allowed selective stimulation of A1AR. AMP-stimulated hypothermia can occur independently of A1AR, A3AR, and mast cells. A1AR and A3AR agonists and AMP cause regulated hypothermia that was characterized by a drop in total energy expenditure, physical inactivity, and preference for cooler environmental temperatures, indicating a reduced body temperature set point. Neither A1AR nor A3AR were required for fasting-induced torpor. A1AR and A3AR agonists and AMP trigger regulated hypothermia via three distinct mechanisms.

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Section: Discussionmentioning

confidence: 99%

Hypothermia in mouse is caused by adenosine A1 and A3 receptor agonists and AMP via three distinct mechanisms

et al. 2017

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“…Our previous studies have shown that Wistar rats given 5′-AMP at a dose of 0.5 g/kg body weight enter a state of torpor approximately 90 min after the injection at an AT of 16°C, and that AIH could downregulate inflammation [14]. In this study, we found that AIH could decrease the levels of CD14, CRP and TLR4 in endotoxemic rats and inhibit the activation of the ERK1/2, p38, NF-κB and JNK pathways.…”

Section: Discussionmentioning

confidence: 61%

“…When administered at a sufficient dose, 5′-AMP allows nonhibernating mammals to rapidly undergo reversible and safe severely hypothermic reactions at ambient temperatures (ATs) of 15-16°C [9][10][11][12][13]. Recently, studies have shown that hypothermia induced by 5′-AMP has an anti-inflammatory effect [10,11,14]. Our previous studies have also shown that hypothermia induced by 5′-AMP could inhibit LPS-induced inflammation [15].…”

Section: Introductionmentioning

confidence: 95%

Adenosine 5′-monophosphate-induced hypothermia inhibits the activation of ERK1/2, JNK, p38 and NF-κB in endotoxemic rats

Wang

Zhang

et al. 2014

International Immunopharmacology

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“…Tan et al [35] showed that higher activity of MMP-9 coexists with higher concentrations of UA and higher IMT. In opposition to the abovementioned results in an experimental animal study performed in rats showed that UA-induced inflammation led to a decrease in MMP-9 activity [36]. Similarly, UA administration during acute phase of ischemic stroke decreased the activity of proinflammatory MMP-9 [37].…”

Section: Discussionmentioning

confidence: 72%

Selected Matrix Metalloproteinases Activity and Hypertension-Mediated Organ Damage in Relation to Uric Acid Serum Level

Gruszka

Rajzer

Dróżdż

et al. 2019

Journal of Hypertension

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Background: Atherosclerosis is as a systemic inflammatory disease associated with the activation of many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity. Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1-2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima-media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper-and normuricemic groups. Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016). Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

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Hypothermia induced by adenosine 5′‐monophosphate attenuates injury in an L‐arginine‐induced acute pancreatitis rat model

Abstract: Hypothermia induced by 5'-AMP could inhibit the acute inflammatory reaction and NF-κB activation associated with acute pancreatitis.

Cited by 12 publications

References 25 publications

Hypothermia in mouse is caused by adenosine A1 and A3 receptor agonists and AMP via three distinct mechanisms

Hypothermia in mouse is caused by adenosine A1 and A3 receptor agonists and AMP via three distinct mechanisms

Adenosine 5′-monophosphate-induced hypothermia inhibits the activation of ERK1/2, JNK, p38 and NF-κB in endotoxemic rats

Selected Matrix Metalloproteinases Activity and Hypertension-Mediated Organ Damage in Relation to Uric Acid Serum Level

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