Publications by authors named "Muthusamy Ganesan"

Amyloid β (Aβ) plaque accumulation-mediated neuronal toxicity has been suggested to cause synaptic damage and consequent degeneration of brain cells in Alzheimer's disease (AD). With the increasing prerequisite of eco-friendly nanoparticles (NPs), research investigators are utilizing green approaches for the synthesis of zinc oxide (ZnO) NPs for pharmaceutical applications. In this present study, ZnO NPs were synthesized from Acanthus ilicifolius to assess the neuroprotective properties in the AD model of transgenic Caenorhabditis elegans strains CL2006 and CL4176 expressing Aβ aggregation.

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Phosphoglycerate mutase 5 (PGAM5) is a Ser/His/Thr phosphatase responsible for regulating mitochondrial homeostasis. Overexpression of PGAM5 is correlated with a poor prognosis in hepatocellular carcinoma, colon cancer, and melanoma. In hepatocellular carcinoma, silencing of PGAM5 reduces growth, which has been attributed to decreased mitophagy and enhanced apoptosis.

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Alzheimer's disease (AD) is an extensive age-associated neurodegenerative disorder. In spite of wide-ranging progress in understanding the AD pathology for the past 50 years, clinical trials based on the hypothesis of amyloid-beta (Aβ) have reserved worsening particularly at late-stage human trials. Consequently, very few old drugs are presently used for AD with inadequate clinical consequences and various side effects.

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In this study, we prepared ferulic acid (FA) and paclitaxel (PTX) co-loaded polyamidoamine (PAMAM) dendrimers conjugated with arginyl-glycyl-aspartic acid (RGD) to overcome P-glycoprotein (P-gp)-mediated multidrug resistance (MDR). FA was released in greater extent (80%) from the outer layer of the dendrimers compared with PTX (70%) from the interior of the dendrimers. FA improved intracellular availability of PTX via P-gp modulation in drug-resistant cells.

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Background: Gold nanoparticles (GNPs) are receiving increasing attention as drug delivery carriers due to their high surface-to-volume ratio, hydrophilicity, and functionality. Drug delivery by nanocarriers has the potential to bypass P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) by altering the drug internalization mechanism and/or intracellular release pattern, inhibiting the activity of ABC-transporter efflux pumps, or downregulating the expression of genes responsible for the activity of efflux pumps.

Objective: We developed a folate-gold-bilirubin (FGB) nanoconjugate to reverse MDR in P-expressing KB-Ch-8-5 cells.

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Correction for 'The preventive effect of linalool on acute and chronic UVB-mediated skin carcinogenesis in Swiss albino mice' by Srithar Gunaseelan, et al., Photochem. Photobiol.

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Aim: The present study was designed to examine the role of alpha-pinene (AP) against skin photoaging in UVA-irradiated mice.

Materials And Methods: Swiss albino mice were subjected to UVA-irradiation at the rate of 10 J/cm per day for ten days, totally mouse received 100 J/cm. One hour prior to each UVA-exposure, the mouse skin was topically treated with AP (100 mg kg/b·wt).

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In this study, the modulatory effect of ferulic acid on P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) was examined in KB Ch8-5 resistant cells and drug-resistant tumor xenografts. We observed that ferulic acid enhanced the cytotoxicity of doxorubicin and vincristine in the P-gp overexpressing KB Ch8-5 cells. Further, ferulic acid enhances the doxorubicin induced γH2AX foci formation and synergistically augmented doxorubicin-induced apoptotic signaling in the drug-resistant cells.

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Oral Squamous Cell Carcinoma (OSCC) patients respond poorly to chemotherapy. We analyzed the expression of 11 drug response-related genes in 31 OSCC biopsies, collected prior to any treatment, using custom-designed PCR array. Further, we investigated the drug response pattern of selected anticancer drugs by BH3 (Bcl2 Homology-3) profiling in the primary cells isolated from OSCC tissues.

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Aims: This study aims to evaluate the protective effect of alpha pinene (AP), an essential oil monoterpene, against ultraviolet-A (UVA; 320-400 nm) induced cellular damages in human skin epidermal keratinocytes (HaCaT cells).

Materials And Methods: In this study, HaCaT cells were subjected to single UVA-irradiation (10 J/cm) in the presence and absence of AP (30 μM) then different cellular end points were analyzed. The protective effect of AP against UVA-induced cytotoxicity was evaluated by MTT-based metabolic assay.

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Previously, we proved that caffeic acid (CA), a major dietary phenolic acid, prevents skin carcinogenesis by modulating inflammatory signaling in mouse skin. However, the actual mechanisms of CA against UVB (280-320 nm) induced photocarcinogenesis remains unclear. The present results confirms that CA significantly inhibits single UVB-induced CPDs formation, oxidative DNA damage, ROS generation and frequency of apoptotic cell death in human dermal fibroblasts (HDFa).

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Ultraviolet-B radiation (285-320 nm) elicits a number of cellular signaling elements. We investigated the preventive effect of linalool, a natural monoterpene, against UVB-induced oxidative imbalance, activation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling in HDFa cells. We observed that linalool treatment (30 μM) prevented acute UVB-irradiation (20 mJ/cm2) mediated loss of activities of antioxidant enzymes in HDFa cells.

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Multidrug resistance (MDR) remains a major obstacle in cancer chemotherapy. The use of the dietary phytochemicals as chemosensitizing agents to enhance the efficacy of conventional cytostatic drugs has recently gained the attention as a plausible approach for overcoming the drug resistance. The aim of this study was to investigate whether a naturally occurring diet-based phenolic acid, ferulic acid, could sensitize paclitaxel efficacy in ABCB1 overexpressing (P-glycoprotein) colchicine selected KB Ch(R)8-5 cell line.

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In this study, we evaluated the role of linalool in acute ultraviolet-B (UVB; 280-320 nm) radiation-induced inflammation and chronic UVB-mediated photocarcinogenesis in mouse skin. Acute UVB-irradiation (180 mJ cm(-2)) causes hyperplasia, edema formation, lipid peroxidation, antioxidant depletion, and overexpression of cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC) in mouse skin. Topical or intraperitoneal (i.

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Ultraviolet B (UVB) irradiation alters multiple molecular pathways in the skin, thereby inducing skin damage. Human dermal fibroblasts (HDFa) were subjected to single UVB-irradiation (18mJ/cm(2)) resulting in reactive oxygen species (ROS) generation, oxidative DNA damage and upregulation of nuclear factor kappa B (NF-κB) expression. Further, it has been observed that there was a significant cytokine production (TNF-α and IL-6) in UVB irradiated HDFa cells.

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Signal transducers and activators of transcription 3 (STAT3) play a critical role in inflammation, proliferation and carcinogenesis. Inhibition of JAK-STAT3 signaling is proved to be a novel target for prevention of UVB-induced skin carcinogenesis. In this study, chronic UVB irradiation (180 mJ cm(-2) ; weekly thrice for 30 weeks) induces the expression of IL-10 and JAK1 that eventually activates the STAT3 which leads to the transcription of proliferative and antiapoptotic markers such as PCNA, Cyclin-D1, Bcl2 and Bcl-xl, respectively.

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Cancer is a hyperproliferative disorder that involves transformation, dysregulation of apoptosis, proliferation, invasion, angiogenesis and metastasis. During the last 30 years, extensive research has revealed much about the biology of cancer. Chemotherapy and radiotherapy are the mainstays of cancer treatment, particularly for patients who do not respond to surgical resection.

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In this study, the effect of caffeic acid (CA) on both acute and chronic UVB-irradiation-induced inflammation and photocarcinogenesis was investigated in Swiss albino mice. Animals were exposed to 180 mJ cm(-2) of UVB once daily for 10 consecutive days and thrice weekly for 30 weeks for acute and chronic study respectively. UVB exposure for 10 consecutive days showed edema formation, increased lipid peroxidation and decreased antioxidant status with activation of inflammatory molecules such as TNF-α, IL-6, COX-2 and NF-κB.

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Objective: To assess the nutritional status of critically ill patients with acute renal failure on continuous renal replacement therapy (CRRT) and their protein needs by estimating the protein equivalent of nitrogen appearance (PNA).

Design: Prospective, observational study.

Setting: A 74-bed intensive care unit in a single tertiary care hospital.

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