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1دورية أكاديمية
المؤلفون: Deepak, Veeraiyan Nallaswamy1, Lakshminarayan, Arivarasu2, 1, Anitha, Roy2, Rajeshkumar, S.2, Lakshmi, Thangavelu2, Ezhilarasan, Devaraj2, Subha, M.3
المصدر: Indian Journal of Public Health Research & Development 10(11):3706-3710. 2019
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2دورية أكاديمية
المؤلفون: Deepak, Veeraiyan Nallaswamy1, Lakshminarayanan, Arivarasu2, 1, Roy, Anitha2, Rajeshkumar, S.2, Lakshmi, Thangavelu2, Ezhilarasan, Devaraj2, Subha, M.3
المصدر: Indian Journal of Public Health Research & Development 10(11):3701-3705. 2019
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3دورية أكاديمية
المؤلفون: Nallaswamy, V. Deepak1, Roy, Anitha2, 1, Rajeshkumar, S.2, Lakshmi, Thangavelu2, Ezhilarasan, Devaraj2, Subha, M.3
المصدر: Indian Journal of Public Health Research & Development 10(11):3692-3695. 2019
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4دورية أكاديمية
المؤلفون: Nallaswamy, V. Deepak1, Roy, Anitha2, 1, Rajeshkumar, S.2, Lakshmi, Thangavelu2, Ezhilarasan, Devaraj2, Subha, M.3
المصدر: Indian Journal of Public Health Research & Development 10(11):3687-3691. 2019
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5كتاب
المؤلفون: Abd-Elsalam, Kamel A., AboDalam, Hussien, Anbukumaran, A., Adil, Syed Farooq, Ahmed, Farah K., Ahmed, Manal M., Ahuja, Vishal, Akhayere, Evidence, Alghuthaymi, Mousa A., Anand, R.S., Ashfaq, Mohammad, Badawy, Marwa T., Balusamy, Sri Renuakdevi, Basit, Abdul, Behera, Anindita, Bejjani, Rami, Reddy G., Bhagavanth, Chaudhry, Amna, Chauhan, Divya, Chelliah, Parvathiraja, Danaraj, Jeyapragash, David, Muniswamy, Devra, Vijay, Dua, Kamal, Ekennia, Anthony C., Elangovan, Ramya Dinesh, Elemike, Elias E., Ezeani, Rachael O., Ezhilarasan, Devaraj, Jeevitha, M., Joseph, John, Kalarikkal, Nandakumar, Kalia, Anu, Kanniah, Paulkumar, Karuppieh, Santhiya, Kasi, Murugan, Kavaz, Doga, Kaviya, A., Keshu, Khalil, Mohamed S., Khan, Mujeeb, Kim, Yeon Ju, Lakshmi, T., Li, Bin, Malhotra, Satinder Pal Kaur, Malyla, Vamshikrishna, Mangalaraja, R.V., Meenu, Mohamed, Heba I., Mostafa, Manal
المصدر: Agri-Waste and Microbes for Production of Sustainable Nanomaterials ; page xxi-xxviii
الإتاحة: https://doi.org/10.1016/b978-0-12-823575-1.09991-1Test
https://api.elsevier.com/content/article/PII:B9780128235751099911?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:B9780128235751099911?httpAccept=text/plainTest -
6دورية أكاديمية
المصدر: Journal of Biochemical and Molecular Toxicology ; volume 38, issue 4 ; ISSN 1095-6670 1099-0461
الوصف: Sustained liver injuries predominantly promote oxidative stress and inflammation that lead to the progression of chronic liver disease (CLD), including fibrosis, cirrhosis, and hepatocellular carcinoma. Boldine, an alkaloid isolated from Peumus boldus , has been shown to have antioxidant and anti‐inflammatory effects. Currently, there is no definitive treatment option available for CLD. Therefore, we investigated the hepatoprotective effect of boldine against carbon tetrachloride (CCl 4 )‐induced chronic liver injury in rats. CCl 4 (2 mL/kg., b.w., i.p.) was administered twice weekly for 5 weeks to induce chronic liver injury in rats. Separate groups of rats were given boldine (20 mg/kg b.w., and 40 mg/kg b.w.) and silymarin (100 mg/kg b.w.) orally, daily. Serum transaminases, lipid peroxidation, and antioxidant levels were measured, and nuclear factor‐κB (NF‐κB), tumor necrosis factor‐α (TNF‐α), cyclooxygenase‐2 (cox‐2), interleukin‐1 β (IL‐1β), and α‐smooth muscle actin (α‐SMA) gene and protein expressions were evaluated. CCl 4 administration increased liver marker enzymes of hepatotoxicity in serum and oxidative stress markers, inflammatory genes and α‐smooth muscle actin expression in liver tissue. Boldine concurrent treatment suppressed CCl 4 ‐induced elevation of transaminase levels in serum, restored enzymic and non‐enzymic antioxidants, and downregulated NF‐κB, TNF‐α, Cox‐2 and IL‐1β expressions, thereby suppressing hepatic inflammation. Boldine administration also repressed α‐SMA expression. The results of this study demonstrate the antioxidant, anti‐inflammatory, and antifibrotic properties of boldine, and it can be a potential therapeutic candidate in the treatment of CLD.
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7دورية أكاديمية
المصدر: Journal of Biochemical and Molecular Toxicology ; volume 38, issue 4 ; ISSN 1095-6670 1099-0461
الوصف: Chronic liver injury due to various etiological factors results in excess secretion and accumulation of extracellular matrix proteins, leading to scarring of liver tissue and ultimately to hepatic fibrosis. If left untreated, fibrosis might progress to cirrhosis and even hepatocellular carcinoma. Thymoquinone (TQ), an active compound of Nigella sativa , has been reported to exhibit antioxidant, anti‐inflammatory and anticancer activities. Therefore, the effect of TQ against thioacetamide (TAA)‐induced liver fibrosis was assessed in rats. Fibrosis was induced with intraperitoneal administration of TAA (250 mg/kg b.w.) twice a week for 5 weeks. TQ (20 mg/kg b.w.) and silymarin (50 mg/kg b.w.) were orally administered daily for 5 weeks separately in TAA administered groups. Liver dysfunction was reported by elevated liver enzymes, increased oxidative stress, inflammation and fibrosis upon TAA administration. Our study demonstrated that TQ inhibited the elevation of liver marker enzymes in serum. TQ administration significantly increased antioxidant markers, such as superoxide dismutase, catalase, glutathione, glutathione peroxidase and glutathione reductase in the liver tissue of rats. Further, TQ significantly attenuated liver fibrosis, as illustrated by the downregulation of TAA‐induced interleukin‐β, tumour necrosis factor‐α, inducible nitric oxide synthase and fibrosis markers like transforming growth factor‐β (TGF‐β), α‐smooth muscle actin, collagen‐1, Smad3 and 7. Therefore, these findings suggest that TQ has a promising hepatoprotective property, as indicated by its potential to effectively suppress TAA‐induced liver fibrosis in rats by inhibiting oxidative stress and inflammation via TGF‐β/Smad signaling.
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8دورية أكاديمية
المصدر: Oral Diseases ; ISSN 1354-523X 1601-0825
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9دورية أكاديمية
المصدر: Cell Biochemistry and Function ; volume 42, issue 1 ; ISSN 0263-6484 1099-0844
الوصف: Alcoholic liver disease (ALD) is one of the most common health problems worldwide, especially in developing countries caused by chronic consumption of alcohol on a daily basis. The ALD spectrum is initiated with the early stages of alcoholic fatty liver (steatosis), progressing to alcoholic steatohepatitis, followed by the later stages of fibrosis and in some cases, cirrhosis and hepatocellular carcinoma (HCC). The Wnt/β‐catenin signaling required for healthy liver development, function, and regeneration is found to be aberrated in ALD, attributed to its progression. This review is to elucidate the association of Wnt/β‐catenin signaling with various stages of ALD progression. Alcohol causes downregulation of Wnt/β‐catenin signaling components and thereby suppressing the pathway. Reports have been published that aberrated Wnt/β‐catenin signaling, especially the absence of β‐catenin, results in decreased alcohol metabolism, causing steatosis followed by steatohepatitis via lipid accumulation, lipid peroxidation, liver injury, increased oxidative stress and apoptosis of hepatocytes, contributing to the advancement of ALD. Contrastingly, the progression of later stages of ALD like fibrosis and HCC depends on the increased activation of Wnt/β‐catenin signaling and its components. Existing studies reveal the varied expression of Wnt/β‐catenin signaling in ALD. However, the dual role of the Wnt/β‐catenin pathway in earlier and later stages of ALD is not clear. Therefore, studies on the Wnt/β‐catenin pathway and its components in various manifestations of ALD might provide insight in targeting the Wnt/β‐catenin pathway in ALD treatment.
الإتاحة: https://doi.org/10.1002/cbf.3916Test
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10دورية أكاديمية
