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The effects of A2B receptor modulators on vascular endothelial growth factor and nitric oxide axis in chronic cyclosporine nephropathy.

Patel L, Thaker A - J Pharmacol Pharmacother (2015 Jul-Sep)

Bottom Line: The analysis of mRNA expression of A2B receptor and VEGF was performed.The effects of A2B AR modulators were prominent in CsA-treated animals compared with control animals suggesting CsA treatment may upregulate A2B ARs.The mRNA expression of A2B AR was increased after 5 weeks of CsA.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, Anand, Gujarat, India.

ABSTRACT

Introduction: To investigate the actions of adenosine A2B receptor modulators on VEGF and NO levels in CsA nephropathy.

Materials and methods: Nephropathy was induced by administrating 25 mg/kg (s.c) of CsA for 5 weeks. The VEGF and NO levels were measured in kidney tissue. Serum creatinine, creatinine clearance, urinary albumin excretion, blood urea nitrogen, kidney pathology score were measured to assess renal function. The analysis of mRNA expression of A2B receptor and VEGF was performed.

Results: Administration of CsA for 5 weeks induced adverse renal function. The mRNA expression of VEGF was reduced in renal tissue after 5 weeks of CsA treatment. The renal VEGF and NO levels were also reduced in these animals. In vivo administration of A2B adenosine receptor agonist increased renal VEGF which was inhibited by a selective A2B AR antagonist (MRS1754) in CsA-treated animals. The increase in VEGF was associated with reversal of adverse renal functions. The effects of A2B AR modulators were prominent in CsA-treated animals compared with control animals suggesting CsA treatment may upregulate A2B ARs. The mRNA expression of A2B AR was increased after 5 weeks of CsA.

Conclusions: A2B AR modulators may provide new therapeutic options to retard CsA nephropathy by mediating renal VEGF and NO.

No MeSH data available.


Related in: MedlinePlus

(a) Expression of A2B receptor mRNA. *P < 0.05 vs. control group. (b) Histopathological characteristics of kidney tissue. The kidney tissues were stained by hematoxylin-eosin and Masson trichrome reagent. (b) Collapsing glomerulopathy. (c) Collagen deposition. (d) arterioplar hylinosis. (e) tubulointerstitial fibrosis seen in CsA nephropathy at original magnification of 400X
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Figure 5: (a) Expression of A2B receptor mRNA. *P < 0.05 vs. control group. (b) Histopathological characteristics of kidney tissue. The kidney tissues were stained by hematoxylin-eosin and Masson trichrome reagent. (b) Collapsing glomerulopathy. (c) Collagen deposition. (d) arterioplar hylinosis. (e) tubulointerstitial fibrosis seen in CsA nephropathy at original magnification of 400X

Mentions: CsA administration induced striped renal injury that included damage to tubular epithelial cells, inflammatory infiltrates, and tubulointerstitial expansion accompanied by fibrosis which was calculated as a kidney pathology score [Figure 4a]. The score was increased in animals treated with CsA. NECA inhibited the pathological changes. Administration of antagonist inhibited the effect of NECA. The expression of VEGF and kidney pathology score were positively correlated [Figure 4b]. The characteristic features of CsA nephropathy are presented in Figure 5b-e.


The effects of A2B receptor modulators on vascular endothelial growth factor and nitric oxide axis in chronic cyclosporine nephropathy.

Patel L, Thaker A - J Pharmacol Pharmacother (2015 Jul-Sep)

(a) Expression of A2B receptor mRNA. *P < 0.05 vs. control group. (b) Histopathological characteristics of kidney tissue. The kidney tissues were stained by hematoxylin-eosin and Masson trichrome reagent. (b) Collapsing glomerulopathy. (c) Collagen deposition. (d) arterioplar hylinosis. (e) tubulointerstitial fibrosis seen in CsA nephropathy at original magnification of 400X
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4544136&req=5

Figure 5: (a) Expression of A2B receptor mRNA. *P < 0.05 vs. control group. (b) Histopathological characteristics of kidney tissue. The kidney tissues were stained by hematoxylin-eosin and Masson trichrome reagent. (b) Collapsing glomerulopathy. (c) Collagen deposition. (d) arterioplar hylinosis. (e) tubulointerstitial fibrosis seen in CsA nephropathy at original magnification of 400X
Mentions: CsA administration induced striped renal injury that included damage to tubular epithelial cells, inflammatory infiltrates, and tubulointerstitial expansion accompanied by fibrosis which was calculated as a kidney pathology score [Figure 4a]. The score was increased in animals treated with CsA. NECA inhibited the pathological changes. Administration of antagonist inhibited the effect of NECA. The expression of VEGF and kidney pathology score were positively correlated [Figure 4b]. The characteristic features of CsA nephropathy are presented in Figure 5b-e.

Bottom Line: The analysis of mRNA expression of A2B receptor and VEGF was performed.The effects of A2B AR modulators were prominent in CsA-treated animals compared with control animals suggesting CsA treatment may upregulate A2B ARs.The mRNA expression of A2B AR was increased after 5 weeks of CsA.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, Anand, Gujarat, India.

ABSTRACT

Introduction: To investigate the actions of adenosine A2B receptor modulators on VEGF and NO levels in CsA nephropathy.

Materials and methods: Nephropathy was induced by administrating 25 mg/kg (s.c) of CsA for 5 weeks. The VEGF and NO levels were measured in kidney tissue. Serum creatinine, creatinine clearance, urinary albumin excretion, blood urea nitrogen, kidney pathology score were measured to assess renal function. The analysis of mRNA expression of A2B receptor and VEGF was performed.

Results: Administration of CsA for 5 weeks induced adverse renal function. The mRNA expression of VEGF was reduced in renal tissue after 5 weeks of CsA treatment. The renal VEGF and NO levels were also reduced in these animals. In vivo administration of A2B adenosine receptor agonist increased renal VEGF which was inhibited by a selective A2B AR antagonist (MRS1754) in CsA-treated animals. The increase in VEGF was associated with reversal of adverse renal functions. The effects of A2B AR modulators were prominent in CsA-treated animals compared with control animals suggesting CsA treatment may upregulate A2B ARs. The mRNA expression of A2B AR was increased after 5 weeks of CsA.

Conclusions: A2B AR modulators may provide new therapeutic options to retard CsA nephropathy by mediating renal VEGF and NO.

No MeSH data available.


Related in: MedlinePlus