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Benfotiamine

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Kota V Ramana – 1st expert on this subject based on the ideXlab platform

  • anti inflammatory effects of Benfotiamine are mediated through the regulation of the arachidonic acid pathway in macrophages
    Free Radical Biology and Medicine, 2012
    Co-Authors: Mohammad Shoeb, Kota V Ramana

    Abstract:

    Abstract Benfotiamine, a lipid-soluble analogue of vitamin B1, is a potent antioxidant that is used as a food supplement for the treatment of diabetic complications. Our recent study (U.C. Yadav et al., Free Radic. Biol. Med. 48:1423–1434, 2010) indicates a novel role for Benfotiamine in the prevention of bacterial endotoxin, lipopolysaccharide (LPS)-induced cytotoxicity and inflammatory response in murine macrophages. Nevertheless, it remains unclear how Benfotiamine mediates anti-inflammatory effects. In this study, we investigated the anti-inflammatory role of Benfotiamine in regulating arachidonic acid (AA) pathway-generated inflammatory lipid mediators in RAW264.7 macrophages. Benfotiamine prevented the LPS-induced activation of cPLA2 and release of AA metabolites such as leukotrienes, prostaglandin E2, thromboxane 2 (TXB2), and prostacyclin (PGI2) in macrophages. Further, LPS-induced expression of AA-metabolizing enzymes such as COX-2, LOX-5, TXB synthase, and PGI2 synthase was significantly blocked by Benfotiamine. Furthermore, Benfotiamine prevented the LPS-induced phosphorylation of ERK1/2 and expression of transcription factors NF-κB and Egr-1. Benfotiamine also prevented the LPS-induced oxidative stress and protein–HNE adduct formation. Most importantly, compared to specific COX-2 and LOX-5 inhibitors, Benfotiamine significantly prevented LPS-induced macrophage death and monocyte adhesion to endothelial cells. Thus, our studies indicate that the dual regulation of the COX and LOX pathways in AA metabolism could be a novel mechanism by which Benfotiamine exhibits its potential anti-inflammatory response.

  • abstract 2397 fat soluble vitamin b1 analogue Benfotiamine prevents colon cancer cell growth and aberrant crypt foci formation in murine models of colon cancer
    Cancer Research, 2011
    Co-Authors: Kota V Ramana, Ashish Saxena, Ravinder Tammali, Aramati B M Reddy, Satish K Srivastava

    Abstract:

    Chronic inflammatory diseases and oxidative stress are major risk factors of colorectal cancer (CRC), the third most common cause of death among cancer patients. Although several agents such as antioxidants, plant products and nutritional supplements have been shown to have some chemopreventive effects on colon cancer, none are very effective to completely. Recent studies indicate that a fat soluble analogue of vitamin B1, Benfotiamine is an excellent antioxidant and anti-inflammatory. However, the chemo-preventive or -therapeutic efficacy of Benfotiamine in preventing CRC is not known. Our hypothesis is that Benfotiamine through its anti-oxidant and anti-inflammatory properties could be very effective in preventing CRC. We therefore investigated the role of Benfotiamine in the prevention of carcinogenic signals leading to CRC in cell culture as well as murine models of CRC. Our results show that treatment of human colon cancer cells (HT-29 and Caco-2) in culture with Benfotiamine prevented the cancer cell proliferation. Further, Benfotiamine also prevented the growth of human adenocarcinoma cells (SW480) -induced tumor growth in nude mice xenografts. Our studies also indicate that Benfotiamine prevented NF-kB-dependent survival signals and activated caspase-3 dependent apoptotic signals in colon cancer cells. Further, Benfotiamine supplementation also suppressed azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation in mice and AOM-induced inflammatory changes such as activation of Cox-2 and iNOS, and carcinogenic changes such as expression of cyclin D1 and β-catenin in mice colons. In conclusion, our results indicate that Benfotiamine prevents colon cancer cell growth in culture and nude mice xenografts as well as formation of ACF in AOM-treated mice. Thus Benfotiamine supplementation could be used as an excellent chemopreventive agent for the treatment of CRC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2397. doi:10.1158/1538-7445.AM2011-2397

  • protective role of Benfotiamine a fat soluble vitamin b1 analogue in lipopolysaccharide induced cytotoxic signals in murine macrophages
    Free Radical Biology and Medicine, 2010
    Co-Authors: Umesh C S Yadav, Satish K Srivastava, Nilesh M Kalariya, Kota V Ramana

    Abstract:

    Abstract This study was designed to investigate the molecular mechanisms by which Benfotiamine, a lipid-soluble analogue of vitamin B1, affects lipopolysaccharide (LPS)-induced inflammatory signals leading to cytotoxicity in the mouse macrophage cell line RAW264.7. Benfotiamine prevented LPS-induced apoptosis, expression of the Bcl-2 family of proapoptotic proteins, caspase-3 activation, and PARP cleavage and altered mitochondrial membrane potential and release of cytochrome c and apoptosis-inducing factor and phosphorylation and subsequent activation of p38-MAPK, stress-activated kinases (SAPK/JNK), protein kinase C, and cytoplasmic phospholipase A2 in RAW cells. Further, phosphorylation and degradation of inhibitory κB and consequent activation and nuclear translocation of the redox-sensitive transcription factor NF-κB were significantly prevented by Benfotiamine. The LPS-induced increased expression of cytokines and chemokines and the inflammatory marker proteins iNOS and COX-2 and their metabolic products NO and PGE2 was also blocked significantly. Thus, our results elucidate the molecular mechanism of the anti-inflammatory action of Benfotiamine in LPS-induced inflammation in murine macrophages. Benfotiamine suppresses oxidative stress-induced NF-κB activation and prevents bacterial endotoxin-induced inflammation, indicating that vitamin B1 supplementation could be beneficial in the treatment of inflammatory diseases.

Umesh C S Yadav – 2nd expert on this subject based on the ideXlab platform

  • original contributionprotective role of Benfotiamine a fat soluble vitamin b1 analogue in lipopolysaccharide induced cytotoxic signals in murine macrophages
    Free Radical Biology and Medicine, 2010
    Co-Authors: Umesh C S Yadav, Satish K Srivastava, Nilesh M Kalariya, Kota V Ramana

    Abstract:

    This study was designed to investigate the molecular mechanisms by which Benfotiamine, a lipid-soluble analogue of vitamin B1, affects lipopolysaccharide (LPS)-induced inflammatory signals leading to cytotoxicity in the mouse macrophage cell line RAW264.7. Benfotiamine prevented LPS-induced apoptosis, expression of the Bcl-2 family of proapoptotic proteins, caspase-3 activation, and PARP cleavage and altered mitochondrial membrane potential and release of cytochrome c and apoptosis-inducing factor and phosphorylation and subsequent activation of p38-MAPK, stress-activated kinases (SAPK/JNK), protein kinase C, and cytoplasmic phospholipase A2 in RAW cells. Further, phosphorylation and degradation of inhibitory κB and consequent activation and nuclear translocation of the redox-sensitive transcription factor NF-κB were significantly prevented by Benfotiamine. The LPS-induced increased expression of cytokines and chemokines and the inflammatory marker proteins iNOS and COX-2 and their metabolic products NO and PGE2 was also blocked significantly. Thus, our results elucidate the molecular mechanism of the anti-inflammatory action of Benfotiamine in LPS-induced inflammation in murine macrophages. Benfotiamine suppresses oxidative stress-induced NF-κB activation and prevents bacterial endotoxin-induced inflammation, indicating that vitamin B1 supplementation could be beneficial in the treatment of inflammatory diseases.

  • protective role of Benfotiamine a fat soluble vitamin b1 analogue in lipopolysaccharide induced cytotoxic signals in murine macrophages
    Free Radical Biology and Medicine, 2010
    Co-Authors: Umesh C S Yadav, Satish K Srivastava, Nilesh M Kalariya, Kota V Ramana

    Abstract:

    Abstract This study was designed to investigate the molecular mechanisms by which Benfotiamine, a lipid-soluble analogue of vitamin B1, affects lipopolysaccharide (LPS)-induced inflammatory signals leading to cytotoxicity in the mouse macrophage cell line RAW264.7. Benfotiamine prevented LPS-induced apoptosis, expression of the Bcl-2 family of proapoptotic proteins, caspase-3 activation, and PARP cleavage and altered mitochondrial membrane potential and release of cytochrome c and apoptosis-inducing factor and phosphorylation and subsequent activation of p38-MAPK, stress-activated kinases (SAPK/JNK), protein kinase C, and cytoplasmic phospholipase A2 in RAW cells. Further, phosphorylation and degradation of inhibitory κB and consequent activation and nuclear translocation of the redox-sensitive transcription factor NF-κB were significantly prevented by Benfotiamine. The LPS-induced increased expression of cytokines and chemokines and the inflammatory marker proteins iNOS and COX-2 and their metabolic products NO and PGE2 was also blocked significantly. Thus, our results elucidate the molecular mechanism of the anti-inflammatory action of Benfotiamine in LPS-induced inflammation in murine macrophages. Benfotiamine suppresses oxidative stress-induced NF-κB activation and prevents bacterial endotoxin-induced inflammation, indicating that vitamin B1 supplementation could be beneficial in the treatment of inflammatory diseases.

  • prevention of endotoxin induced uveitis in rats by Benfotiamine a lipophilic analogue of vitamin b1
    Investigative Ophthalmology & Visual Science, 2009
    Co-Authors: Umesh C S Yadav, Sumitra Subramanyam, Kota V Ramana

    Abstract:

    PURPOSE: To study the amelioration of ocular inflammation in endotoxin-induced uveitis (EIU) in rats by Benfotiamine, a lipid-soluble analogue of thiamine. METHODS: EIU in Lewis rats was induced by subcutaneous injection of lipopolysaccharide (LPS) followed by treatment with Benfotiamine. The rats were killed 3 or 24 hours after LPS injection, eyes were enucleated, aqueous humor (AqH) was collected, and the number of infiltrating cells, protein concentration, and inflammatory marker levels were determined. Immunohistochemical analysis of eye sections was performed to determine the expression of inducible-nitric oxide synthase (iNOS), cyclooxygenase (Cox)-2, protein kinase C (PKC), and transcription factor NF-kappaB. RESULTS: Infiltrating leukocytes, protein concentrations, and inflammatory cytokines and chemokines were significantly elevated in the AqH of EIU rats compared with control rats, and Benfotiamine treatment suppressed these increases. Similarly increased expression of inflammatory markers iNOS and Cox-2 in ciliary body and retinal wall was also significantly inhibited by Benfotiamine. The increased phosphorylation of PKC and the activation of NF-kappaB in the ciliary body and in the retinal wall of EIU rat eyes were suppressed by Benfotiamine. CONCLUSIONS: These results suggest that Benfotiamine suppresses oxidative stress-induced NF-kappaB-dependent inflammatory signaling leading to uveitis. Therefore, Benfotiamine could be used as a novel therapeutic agent for the treatment of ocular inflammation, especially uveitis.

Pitchai Balakumar – 3rd expert on this subject based on the ideXlab platform

  • the defensive effect of Benfotiamine in sodium arsenite induced experimental vascular endothelial dysfunction
    Biological Trace Element Research, 2010
    Co-Authors: Sanjali Verma, Krishna Reddy, Pitchai Balakumar

    Abstract:

    The present study has been designed to investigate the effect of Benfotiamine, a thiamine derivative, in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Sodium arsenite (1.5 mg−1 kg−1 day−1 i.p., 2 weeks) was administered in rats to produce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating the serum and aortic concentrations of nitrite/nitrate. Further, the integrity of vascular endothelium in thoracic aorta was assessed by scanning electron microscopy. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of sodium arsenite markedly produced VED by attenuating acetylcholine-induced endothelium-dependent relaxation, decreasing serum and aortic concentrations of nitrite/nitrate, and impairing the integrity of vascular endothelium. Further, sodium arsenite produced oxidative stress by increasing serum TBARS and aortic superoxide generation. The treatment with Benfotiamine (25, 50, and 100 mg−1 kg−1 day−1 p.o.) or atorvastatin (30 mg−1 kg−1 day−1 p.o., a standard agent) prevented sodium arsenite-induced VED and oxidative stress. However, the beneficial effects of Benfotiamine in preventing the sodium arsenite-induced VED were attenuated by co-administration with N-omega-nitro-l-arginine methyl ester (L-NAME) (25 mg−1 kg−1 day−1, i.p.), an inhibitor of NOS. Thus, it may be concluded that Benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.

  • the multifaceted therapeutic potential of Benfotiamine
    Pharmacological Research, 2010
    Co-Authors: Pitchai Balakumar, Ankur Rohilla, Pawan Krishan, P Solairaj, Arunachalam Thangathirupathi

    Abstract:

    Thiamine, known as vitamin B1, plays an essential role in energy metabolism. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine. Once absorbed, Benfotiamine is dephosphorylated by ecto-alkaline phosphatase to lipid-soluble S-benzoylthiamine. Transketolase is an enzyme that directs the precursors of advanced glycation end products (AGEs) to pentose phosphate pathway. Benfotiamine administration increases the levels of intracellular thiamine diphosphate, a cofactor necessary for the activation transketolase, resulting in the reduction of tissue level of AGEs. The elevated level of AGEs has been implicated in the induction and progression of diabetes-associated complications. Chronic hyperglycemia accelerates the reaction between glucose and proteins leading to the formation of AGEs, which form irreversible cross-links with many macromolecules such as collagen. In diabetes, AGEs accumulate in tissues at an accelerated rate. Experimental studies have elucidated that binding of AGEs to their specific receptors (RAGE) activates mainly monocytes and endothelial cells and consequently induces various inflammatory events. Moreover, AGEs exaggerate the status of oxidative stress in diabetes that may additionally contribute to functional changes in vascular tone control observed in diabetes. The anti-AGE property of Benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Interestingly, few recent studies demonstrated additional non-AGE-dependent pharmacological actions of Benfotiamine. The present review critically analyzed the multifaceted therapeutic potential of Benfotiamine.

  • The multifaceted therapeutic potential of Benfotiamine
    Pharmacological Research, 2010
    Co-Authors: Pitchai Balakumar, Ankur Rohilla, Pawan Krishan, P Solairaj, Arunachalam Thangathirupathi

    Abstract:

    Thiamine, known as vitamin B1, plays an essential role in energy metabolism. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine. Once absorbed, Benfotiamine is dephosphorylated by ecto-alkaline phosphatase to lipid-soluble S-benzoylthiamine. Transketolase is an enzyme that directs the precursors of advanced glycation end products (AGEs) to pentose phosphate pathway. Benfotiamine administration increases the levels of intracellular thiamine diphosphate, a cofactor necessary for the activation transketolase, resulting in the reduction of tissue level of AGEs. The elevated level of AGEs has been implicated in the induction and progression of diabetes-associated complications. Chronic hyperglycemia accelerates the reaction between glucose and proteins leading to the formation of AGEs, which form irreversible cross-links with many macromolecules such as collagen. In diabetes, AGEs accumulate in tissues at an accelerated rate. Experimental studies have elucidated that binding of AGEs to their specific receptors (RAGE) activates mainly monocytes and endothelial cells and consequently induces various inflammatory events. Moreover, AGEs exaggerate the status of oxidative stress in diabetes that may additionally contribute to functional changes in vascular tone control observed in diabetes. The anti-AGE property of Benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Interestingly, few recent studies demonstrated additional non-AGE-dependent pharmacological actions of Benfotiamine. The present review critically analyzed the multifaceted therapeutic potential of Benfotiamine. © 2010 Elsevier Ltd.