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RISS 인기검색어
- 검색키워드
- 저자 : Palanisamy Arulselvan (검색결과 3 건)
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Periyar Selvam Sellamuthu,,Palanisamy Arulselvan,Balu Periamallipatti Muniappan,Sharida Fakurazi,Murugesan Kandasamy 한국식품영양과학회 2013 Journal of medicinal food Vol.16 No.8
Oxidative stress in diabetic tissues is a consequence of free radical accumulation with concurrently impaired natural antioxidants status and results in oxidative tissue damage. The present study investigated the protective effects of mangiferin against pancreatic β-cell damage and on the antioxidant defense systems in streptozotocin (STZ)-induced diabetic rats. Diabetes was experimentally induced by a single intraperitoneal injection of STZ. Oxidative stress biomarkers such as tissue malondialdehyde, hydroperoxides, reduced glutathione (GSH) content, and nonenzymatic antioxidants were measured. Biochemical observations were further substantiated with histological examination and ultrastructural studies in the pancreas of diabetic, glibenclamide and mangiferin-treated diabetic rats (dosage of 40 mg/kg body weight daily for 30 days). Oral administration of mangiferin and glibenclamide to diabetic rats significantly decreased the level of blood glucose and increased levels of insulin. Additionally, mangiferin treatment significantly modulated the pancreatic nonenzymatic antioxidants status (vitamin C, vitamin E, ceruloplasmin, and reduced GSH content) and other oxidative stress biomarkers. The histoarchitecture of diabetic rats showed degenerated pancreas with lower β-cell counts, but mangiferin treatment effectively regenerated insulin secreting islet cells. The electron microscopic study revealed damaged nuclear envelope and mitochondria and fewer secretory granules in pancreas of diabetic rats; however, mangiferin treatment nearly normalized pancreatic architecture. The present findings suggest that mangiferin treatment exerts a therapeutic protective nature in diabetes by decreasing oxidative stress and protecting against pancreatic β-cell damage, which may be attributable to its antioxidative properties.
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SAMER HASAN HUSSEIN-AL-ALI,Palanisamy Arulselvan,Sharida Fakurazi,Maznah Ismail,DENA DORNIANI,MOHD ZOBIR HUSSEIN 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2014 NANO Vol.9 No.2
Magnetic nanoparticles (MNPs) were prepared by the coprecipitation method using a molar ratioof Fe 3 þ:Fe 2 þof 2:1. The surface of MNP was coated with chitosan (CS) and polyethylene glycol(PEG) to form CS – MNP and PEG – MNP nanoparticles, respectively. Anthranilic acid (AA) wasloaded on the surface of the resulting nanoparticles to form AA – CS – MNP and AA – PEG – MNPnanocomposites, respectively. The nanocomposites obtained were characterized using powderX-ray di®raction (XRD), Fourier transform infrared spectroscopy (FTIR), thermogravimetryanalysis (TGA), vibrating sample magnetometer (VSM) and scanning electron microscopy (SEM). XRD results showed that the as-synthesized nanocomposites are pure magnetite. FTIRresults analysis indicated the existence of two polymers on the particle surface of the MNP andthe presence of loaded AA on the surface of CS – MNP and PEG – MNP nanoparticles. Anthranilicacid loading and the release pro¯les of AA – CS – MNP and AA – PEG – MNP nanocompositesshowed that up to 8.8% and 5.5% of the adsorbed drug were released in 670 min and 771 min,respectively. Anthranilic acid release pro¯les followed a pseudo-second-order kinetic controlledprocess. The cytotoxicity of the as-synthesized anthranilic acid nanocomposities were determinedusing MTT assay using murine macrophage RAW 264.7 cells. MTT results showed that thecytotoxic e®ects of AA – CS – MNP were higher than AA – PEG – MNP against the tested cells ascompared to free anthranilic acid. In this manner, this study introduces novel anthranilic acidnanocomposites that can be used on-demand for biomedical applications.
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Jiang, Xu,Ganesan, Palanivel,Rengarajan, Thamaraiselvan,Choi, Dong-Kug,Arulselvan, Palanisamy Elsevier 2018 BIOMEDICINE AND PHARMACOTHERAPY Vol.106 No.-
<P><B>Abstract</B></P> <P>Pathogenesis of Parkinson’s disease (PD) is undoubtedly a multifactorial phenomenon, with diverse etiological agents. Pro-inflammatory mediators act as a skew that directs disease progression during neurodegenerative diseases. Understanding the dynamics of inflammation and inflammatory mediators in preventing or reducing disease progression has recently gained much attention. Inflammatory neuro-degeneration is regulated via cytokines, chemokines, lipid mediators and immune cell subsets; however, individual cellular phenotypes in the Central Nervous System (CNS) acts in diverse ways whose persistent activation leads to unresolving inflammation often causing unfavorable outcomes in neurodegenerative disease like PD. Specifically, activation of cellular phenotypes like astrocytes, microglia, activation of peripheral immune cells requires different activation signals and agents like (cytokines, misfolded protein aggregates, infectious agents, pesticides like organophosphates, etc.,). However, what is unknown is how the different cellular phenotypes respond uniquely and the role of the factors they secrete alters the signal cascades in the complex neuron-microglial connections in the CNS. Hence, understanding the role of cellular phenotypes and the inflammatory mediators, the cross talk among the signals and their receptors can help us to identify the potential therapeutic target using natural products. In this review we have tried to put together the role of cellular phenotypes as a skew that favors PD progression and we have also discussed how the lack of experimental approaches and challenges that affects understanding the cellular targets that can be used against natural derivatives in alleviating PD pathophysiology. Together, this review will provide the better insights into the role of cellular phenotypes of neuroinflammation, inflammatory mediators and the orchestrating factors of inflammation and how they can be targeted in a more specific way that can be used in the clinical management of PD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Distinct cellular Phenotypes acts uniquely in the pathogenesis of PD. </LI> <LI> Inflammation can be cause and consequence of PD pathogenesis. </LI> <LI> Flavonoids regulate multiple modulators of inflammation in mitigating PD pathology. </LI> <LI> Diverse intrinsic/extrinsic mediators converge together in glial activation in exacerbating PD pathology. </LI> </UL> </P>
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