Vijayakumar Natesan

Dr. Vijayakumar Natesan

Biochemistry and Biotechnology, Annamalai University, Chidambaram, India
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Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2018 in Phytochemistry
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Journal Article
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RMRenuka Mani
Renuka Mani
Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan

1 November 2021 in Biomolecules & Therapeutics
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Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan
SKSung-Jin Kim
Sung-Jin Kim
Vijayakumar Natesan and Sung-Jin Kim. Biomolecules & Therapeutics 2021;29:596-604. https://doi.org/10.4062/biomolther.2021.122

23 April 2021 in Biomolecules & Therapeutics
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Journal Article
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Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan
SKSung-Jin Kim
Sung-Jin Kim
Vijayakumar Natesan and Sung-Jin Kim. Biomolecules & Therapeutics 2021;29:365-72. https://doi.org/10.4062/biomolther.2020.204

1 December 2016 in Biomedicine & Pharmacotherapy
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Journal Article
Closed access
VAVenkatesan Amalan
Venkatesan Amalan
Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan
DIDhananjayan Indumathi
Dhananjayan Indumathi
ARArumugam Ramakrishnan
Arumugam Ramakrishnan

1 July 2016 in Biomedicine & Pharmacotherapy
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Journal Article
Closed access
Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan
RMRenuka Mani
Renuka Mani
RARamakrishnan Arumugam
Ramakrishnan Arumugam

23 November 2022 in Metabolites
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Amalan VenkatesanAmalan Venkatesan
Amalan Venkatesan
ARAnitha Roy
Anitha Roy
SKSRINIVASAN KULANDAIVEL
SRINIVASAN KULANDAIVEL
Vijayakumar NatesanVijayakumar Natesan
Vijayakumar Natesan
SKSung-Jin Kim
Sung-Jin Kim
Diabetic nephropathy (DN) has become a leading cause of end-stage renal failure worldwide. The goal of the current study was to examine the protective effects of chitosan-loaded p-Coumaric acid nanoparticles (PCNPs) in nephrotoxicity induced by streptozotocin (STZ). Because of the antidiabetic, anti-inflammatory, and antioxidant properties of PCNPs, the development of DN may be considerably decreased. In this study, the rats received a single intraperitoneal injection (i.p.) of STZ (45 mg/kg) to induce DN. PCNPs were given orally 80 mg/kg b.w to the rats for a duration of four weeks. Body weight, kidney weight, blood glucose, and insulin levels were measured at the end of the experiment. Serum and urine parameters were also examined, along with the histological, immunobiological, and tumor necrosis factor (TNF) and interleukin-6 (IL-6) expression of the nephrotic rats. To comprehend the impact of PCNPs, the expression patterns of the kidney injury molecule (KIM-1) and glucose transporter-2 (GLUT-2) were evaluated. Administration of PCNPs significantly increased body weight, decreased kidney weight and also ameliorated blood glucose levels in the nephropathic rats. The administration of PCNPs also reverted the levels of urea, serum creatinine, urinary NAG, β-glucuronidase and albumin to near-normal levels. The administration of PCNPs also caused the levels of serum and urine parameters to return to near-normal levels. Additionally, the PCNP-treated rats had markedly reduced TNF-α, IL-6, and KIM-1 expressions as well as enhanced GLUT-2 mRNA expression. Our findings clearly showed that PCNP administration prevents the onset of DN in rats by lowering hyperglycemia, decreasing inflammation, and improving the expression of GLUT-2 mRNA in nephropathic rats.