Concentration of tissue angiotensin II increases with severity of experimental pancreatitis

Furukawa, Hiroyuki; Shinmura, Atsushi; Tajima, Hidehiro; Tsukada, Tomoya; Nakanuma, Shinichi; Okamoto, Koichi; Sakai, Seisho; Makino, Isamu; Nakamura, Keisuke; Hayashi, Hironori; Oyama, Katsunobu; Inokuchi, Masafumi; Nakagawara, Hisatoshi; Miyashita, Tomoharu; Fujita, Hideto; Takamura, Hiroyuki; Ninomiya, Itasu; Kitagawa, Hirohisa; Fushida, Sachio; Fujimura, Takashi; Ohta, Tetsuo; Wakayama, Tomohiko; Iseki, Shoichi

doi:10.3892/mmr.2013.1509

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…Ang II and its receptors AT1 and AT2 serve important roles in the pathogenesis of AP, whereas Ang 1–7 has been reported to act as an antagonist that inhibits inflammation ( 16 , 17 ). In addition, recent studies have demonstrated that Ang II can regulate TLR4 expression in order to modulate inflammation and other associated functions ( 18 – 20 ).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin 1-7 ameliorates caerulein-induced inflammation in pancreatic acinar cells by downregulating Toll-like receptor 4/nuclear factor-κB expression

Wang

Cui

et al. 2017

Mol Med Report

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The present study aimed to investigate the effects of angiotensin (Ang) 1–7 on caerulein (CAE)-stimulated nuclear factor (NF)-κB, Toll-like receptor (TLR4) and cytokine expression using pancreatic acinar AR42J cells. AR42J cells were treated with 10 nmol/l CAE for various durations. In addition, cells were pretreated with various concentrations of Ang 1–7 or A779, a specific antagonist of Ang 1–7, and were stimulated with CAE for 12 h. Control cells were treated with vehicle (F-12K complete medium with 2% fetal bovine serum, 10 U/ml penicillin and 100 mg/ml streptomycin) alone. The mRNA and protein expression levels of TLR4, NF-κB, interleukin (IL)-6, IL-8, IL-10 and tumor necrosis factor-α (TNF-α) were determined by western blotting, immunofluorescence and reverse transcription-quantitative polymerase chain reaction. CAE treatment stimulated TLR4 and NF-κB expression within AR42J cells. Immunofluorescence indicated that TLR4 was expressed on the membranes and in the cytoplasm of AR42J cells, whereas NF-κB expression accumulated in the cytoplasm and nuclei. CAE-induced expression of TLR4 and NF-κB within AR42J cells was abrogated by 10−5 mmol/l Ang 1–7; however, TLR4 and NF-κB expression was enhanced with the addition of A779, particularly 10−5 mmol/l. In addition, treatment with 10−6 and 10−5 mmol/l Ang 1–7 significantly mitigated CAE-induced expression of IL-6, IL-8 and TNF-α, whereas it enhanced IL-10 expression. Conversely, A779 treatment enhanced the CAE-induced expression of IL-6, IL-8 and TNF-α, and reduced IL-10 expression in AR42J cells. In conclusion, these results suggested that Ang 1–7 may attenuate CAE-induced inflammation by downregulating TLR4, NF-κB and proinflammatory cytokine expression within AR42J cells. Therefore, Ang 1–7 may exert protective effects against the pathological progression of AP in a cell model of AP induced by CAE and may be considered in the development of treatments for this disease.

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Section: Discussionmentioning

confidence: 99%

Angiotensin 1-7 ameliorates caerulein-induced inflammation in pancreatic acinar cells by downregulating Toll-like receptor 4/nuclear factor-κB expression

Wang

Cui

et al. 2017

Mol Med Report

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“…Frozen tissue samples were homogenized in 0.1% NHCl and 5% urinastatin saline at 4°C. The homogenate was centrifuged for 30 min at 4°C at 10,000 g , with the supernatant collected and analyzed with an enzyme‐linked immunosorbent assay 25 .…”

Section: Methodsmentioning

confidence: 99%

Diet‐induced prediabetes: Effects on the activity of the renin–angiotensin–aldosterone system in selected organs

Mkhize

Mosili

Ngubane

et al. 2022

J of Diabetes Invest

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Aims/Introduction Derangements often observed with type 2 diabetes are associated with disturbances in renin–angiotensin–aldosterone system (RAAS) activity. A positive correlation between local RAAS activity and the complications observed in type 2 diabetes has been noted. However, the detrimental ramifications due to moderate hyperglycemia noted in prediabetes, and the affected organ system and mechanistic pathways are not elucidated. Hence, this study investigated the effects of diet‐induced prediabetes on RAAS in various organs. Materials and Methods Male Sprague–Dawley rats were separated into two groups: (i) non‐prediabetes through exposure to standard rat chow group; and (ii) diet‐induced prediabetes group by exposure to a high‐fat high‐carbohydrate diet for 32 weeks. RAAS activity in the skeletal muscle, adipose tissue, liver, pancreas and heart was determined through the analysis of RAAS components, such as renin, angiotensinogen, angiotensin‐converting enzyme and angiotensin II type 1 receptor through polymerase chain reaction, as well as the quantification of angiotensin II and aldosterone concentration. Furthermore, nicotinamide adenine dinucleotide phosphate oxidase, superoxide dismutase and glutathione peroxidase 1 concentrations were determined in the skeletal muscle, pancreas and heart, in addition to the hepatic triglycerides. Results The RAAS components were elevated in the diet‐induced prediabetes group when compared with the non‐prediabetes group. This was further accompanied by increased nicotinamide adenine dinucleotide phosphate oxidase and reduced superoxide dismutase and glutathione peroxidase 1 concentrations in the selected organs, in addition to the elevated hepatic triglycerides concentration in the diet‐induced prediabetes by comparison to non‐prediabetes group. Conclusions Due to these observed changes, we suggest that local RAAS activity in the prediabetes state in selected organs elicits the derangements noted in type 2 diabetes.

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Angiotensins as therapeutic targets beyond heart disease

Passos‐Silva

Brandan

Santos

2015

Trends in Pharmacological Sciences

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Concentration of tissue angiotensin II increases with severity of experimental pancreatitis

Cited by 3 publications

References 34 publications

Angiotensin 1-7 ameliorates caerulein-induced inflammation in pancreatic acinar cells by downregulating Toll-like receptor 4/nuclear factor-κB expression

Angiotensin 1-7 ameliorates caerulein-induced inflammation in pancreatic acinar cells by downregulating Toll-like receptor 4/nuclear factor-κB expression

Diet‐induced prediabetes: Effects on the activity of the renin–angiotensin–aldosterone system in selected organs

Angiotensins as therapeutic targets beyond heart disease

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