Effects of Vanadate on Expression of Liver Arginase in Experimental Diabetic Rats

Salimuddin,; Upadhyaya, Kailash C.; Baquer, Najma Zaheer

doi:10.1080/152165499307297

Cited by 9 publications

(8 citation statements)

References 15 publications

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“…30,[38][39][40] It should also be noted that p38 MAPK and cAMP 24 pathways regulate arginase expression, and both of these are in turn regulated by SHP2. Intriguingly, SHP2 appeared to positively regulate its own gene expression in an insulin receptor-β and p38 MAPK-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Protein Tyrosine Phosphatase SHP2 Mediates Chronic Insulin-Induced Endothelial Inflammation

Giri

Muthuramu

Dhar

et al. 2012

ATVB

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Objective-Insulin promotes adhesion of leukocytes to the endothelium through increased expression of surface adhesion molecules. We determined whether src-homology domain-2-containing protein tyrosine phosphatase 2 (SHP2), a downstream effecter of insulin signaling, is involved in insulin-induced endothelial inflammation. Methods and Results-In human umbilical vein-derived endothelial cells, treatment with insulin (100 nmol/L) increased Tyr 542 phosphorylation, activity, and subsequently expression of SHP2. Increase in SHP2 accompanied a parallel decrease in the availability of the anti-inflammatory molecule, NO. This consequently enhanced the expression of cell adhesion molecules. Decrease in NO index was caused by endothelial NO synthase (eNOS) uncoupling and increased arginase activity. Among the 2 isoforms, insulin treatment induced the expression of arginase II. Inactivation of endogenous SHP2 via NSC87877 [8-hydroxy-7-(6-sulfonapthalen-2-yl)-diazenyl-quinoline-5-sulfonic acid] and its knockdown by small interfering RNA decreased arginase activity by blocking arginase II expression; however, it failed to restore eNOS coupling. Inactivation of SHP2 also abrogated insulin-mediated leukocyte adhesion by blocking the expression of adhesion molecules. Finally, downregulation of endogenous arginase II blocked insulin-mediated endothelial inflammation. Conclusion-SHP2

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Section: Discussionmentioning

confidence: 99%

Protein Tyrosine Phosphatase SHP2 Mediates Chronic Insulin-Induced Endothelial Inflammation

Giri

Muthuramu

Dhar

et al. 2012

ATVB

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“…The research work of Syed et al (2012) also showed that administration of CCl4 to normal rats increased serum levels of AST, ALT, ALP, and bilirubin. Salimuddin et al (2008) reported that alterations in hepatic function may be because of increase activity and mRNA levels of araginase. These earlier reports therefore made evaluation of ALT, AST, ALP and TP activities necessary for our assessment of hepatocellular dysfunction.…”

Section: Sacrifice Of Animalsmentioning

confidence: 99%

Stem Bark Extracts of <i>Ficus exasperata</i> protects the Liver against Paracetamol induced toxicity in Wistar Rats

Enogieru¹,

Charles²,

Omoruyi³

et al. 2015

Journal of Applied Sciences and Environmental Management

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ABSTRACT:Ficus exasperata is an important medicinal plant with a wide geographical distribution in Africa particularly in Nigeria. In this study, aqueous stem bark extracts of Ficus exasperata were administered to investigate its hepatoprotective effects on Paracetamol induced liver toxicity in Wistar rats. A total of Twenty Five Wistar rats were randomly divided into five groups labeled A-E and kept in a well ventilated room. Group A served as control and were treated with distilled water. Rats in groups B-E were all treated with Paracetamol (800mg/kg body weight) but rats in group C, D and E were however pretreated with Silymarin (50 mg/kg bw), 100mg/kg bw aqueous stem bark extracts of Ficus exasperata and 200mg/kg bw aqueous stem bark extracts of Ficus exasperata respectively one hour before Paracetamol administration for fourteen days. Animals were sacrificed twenty four hours after the last treatment. Blood samples were collected into heparinized bottles for biochemical estimation of liver enzymes and the liver was harvested for routine histological examination. Paracetamol produced significant changes in biochemical parameters (increases in serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP), with a reduction in Total protein) and Liver histology (damage to hepatocytes). Pretreatment with Silymarin and aqueous stem bark extracts of Ficus exasperata significantly prevented the biochemical and histological changes induced by Paracetamol in the liver. In conclusion, our histological and biochemical findings indicate that aqueous stem bark extracts of Ficus exasperata possesses hepatoprotective properties. © JASEM http://dx.doi.org/10.4314/jasem.v19i1.20

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“…Penurunan arginin bisa disebabkan oleh: (1) kebutuhan arginin yang meningkat karena peningkatan ekspresi eNOS yang berhubungan dengan peningkatan moderate oksidasi LDL dan lisofosfatidilkolin. Peningkatan ekspresi eNOS berfungsi sebagai mekanisme pertahanan anti atero-sklerosis pada stadium awal pembentukan lesi aterosklerosis [20]; (2) penghancuran arginin yang meningkat karena: (a) pembentukan arginin-imidazolon adduct, arginin-dehidroimi dazolon adduct dan arginin-lisin croslink karena glikosilasi non-enzimatik meningkat [13], (b) katabolisme arginin yang meningkat karena overekspresi arginase [28][29][30]; (3) gangguan sistem transport arginin yang afinitas tinggi untuk uptake arginin ke dalam sel endotel akibat peningkatan radikal bebas [19,[31][32][33][34]. Maka diperlukan upaya peningkatan L-arginin yang lebih besar dari biasanya untuk mempertahankan uptake arginin ke dalam sel endotel.…”

Section: Stress Oksidatifunclassified

Efek Suplemen L-Arginin Subakut Peroral pada Kontraksi Aorta Tikus Diabetes

Ismail

Ali²,

Soeatmadji

2013

JELS

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Penelitian ini bertujuan untuk mengetahui pengaruh suplemen L-arginin subakut peroral pada tikus diabetesstreptozotosin terhadap respons kontraksi aorta melalui mekanisme pencegahan peningkatan stress oksidatif. Larginine diberikan selama 8 minggu pada tikus diabetes dengan dosis 10, 100 dan 1000 mg.kg-1 BB.hari-1. Parameter yang diukur adalah MDA-plasma untuk menilai oksidatif stress dan teknik bioassay dengan isolasi organ terpisah aorta ring untuk menilai respons reseptor adrenergik- 1 di otot polos aorta terhadap fenilefrin (PE). Dari respons kontraksi aorta dapat diketahui nilai Emaks dan pD 2 PE. Hasil penelitian menunjukkan bahwa pemberian L-arginin 100, 1000 mg.kg-1 BB.hari-1 pada tikus diabetes dapat mencegah peningkatan MDA-plasma (p<0.001). Pemberian L-arginin dosis 100, 1000 mg.kg-1 BB.hari-1 dapat mencegah peningkatan respons kontraksi aorta terhadap PE melalui pencegahan peningkatan Emaks (p<0.000) dan menurunkan pD 2 pada dosis 1000 mg.kg-1 BB.hari-1 (p<0.001). Hasil Jalur Hubungan menunjukkan pencegahan peningkatan Emaks melalui jalur pencegahan peningkatan MDA (p<0.012) dan penurunan pD 2 melalui jalur langsung (p<0.016). Berdasarkan haasil penelitian dapat disimpulkan bahwa pemberian suplemen Larginin pada tikus diabetes dapat mencegah peningkatan respons kontraksi aorta terhadap PE dengan cara: (1) mencegah peningkatan Emaks melalui pencegahan peningkatan MDA (jalur tidak langsung); dan (2) secara langsung menurunkan afinitas reseptor adrenergik- 1 .

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Effects of Vanadate on Expression of Liver Arginase in Experimental Diabetic Rats

Cited by 9 publications

References 15 publications

Protein Tyrosine Phosphatase SHP2 Mediates Chronic Insulin-Induced Endothelial Inflammation

Protein Tyrosine Phosphatase SHP2 Mediates Chronic Insulin-Induced Endothelial Inflammation

Stem Bark Extracts of <i>Ficus exasperata</i> protects the Liver against Paracetamol induced toxicity in Wistar Rats

Efek Suplemen L-Arginin Subakut Peroral pada Kontraksi Aorta Tikus Diabetes

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