다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

Oxidative stress is a normal phenomenon in the body. Under normal conditions, the physiologically important intracellular levels of reactive oxygen species (ROS) are maintained at low levels by various enzyme systems participating in the in vivo redox homeostasis. Therefore, oxidative stress can also be viewed as an imbalance between the prooxidants and antioxidants in the body. For the last two decades, oxidative stress has been one of the most burning topics among the biological researchers all over the world. Several reasons can be assigned to justify its importance: knowledge about reactive oxygen and nitrogen species production and metabolism; identification of biomarkers for oxidative damage; evidence relating manifestation of chronic and some acute health problems to oxidative stress; identification of various dietary antioxidants present in plant foods as bioactive molecules; and so on. This review discusses the importance of oxidative stress in the body growth and development as well as proteomic and genomic evidences of its relationship with disease development, incidence of malignancies and autoimmune disorders, increased susceptibility to bacterial, viral, and parasitic diseases, and an interplay with prooxidants and antioxidants for maintaining a sound health, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue.

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Oxidative Stress, Prooxidants, and Antioxidants: The Interplay

A complex antioxidant system has been developed in mammals to relieve oxidative stress. However, excessive reactive species derived from oxygen and nitrogen may still lead to oxidative damage to tissue and organs. Oxidative stress has been considered as a conjoint pathological mechanism, and it contributes to initiation and progression of liver injury. A lot of risk factors, including alcohol, drugs, environmental pollutants and irradiation, may induce oxidative stress in liver, which in turn results in severe liver diseases, such as alcoholic liver disease and non-alcoholic steatohepatitis. Application of antioxidants signifies a rational curative strategy to prevent and cure liver diseases involving oxidative stress. Although conclusions drawn from clinical studies remain uncertain, animal studies have revealed the promising in vivo therapeutic effect of antioxidants on liver diseases. Natural antioxidants contained in edible or medicinal plants often possess strong antioxidant and free radical scavenging abilities as well as anti-inflammatory action, which are also supposed to be the basis of other bioactivities and health benefits. In this review, PubMed was extensively searched for literature research. The keywords for searching oxidative stress were free radicals, reactive oxygen, nitrogen species, anti-oxidative therapy, Chinese medicines, natural products, antioxidants and liver diseases. The literature, including ours, with studies on oxidative stress and anti-oxidative therapy in liver diseases were the focus. Various factors that cause oxidative stress in liver and effects of antioxidants in the prevention and treatment of liver diseases were summarized, questioned, and discussed.

/pdf/the-role-of-oxidative-stress-and-antioxidants-in-liver-3pnddyz5af.pdf

The Role of Oxidative Stress and Antioxidants in Liver Diseases

PdCl 2 -catalyzed synthesis of a new class of isocoumarin derivatives containing aminosulfonyl / aminocarboxamide moiety: First identification of a isocoumarin based PDE4 inhibitor.

Gouty arthritis is an extremely painful, intense, acute inflammatory disorder that erupts in response to articular deposits of monosodium urate (MSU) crystals. Apart from pain management, therapeutic approaches target at suppressing the inflammation. In the present study, we evaluated the efficacy of 6- Gingerol (25mg/kg b. wt) against monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis. The non-steroidal anti-inflammatory drug, indomethacin (3 mg/kg body weight) was used as a reference for comparison. Paw volume and levels/activities of lysosomal enzymes were assessed in control and monosodium urate crystal-induced mice. In addition, polymorphonuclear leucocytes (PMNL) incubated with monosodium urate crystals in vitro were also examined for the levels of acid phosphatase and lactate dehydrogenase released. Increase in levels of lysosomal enzymes, and paw volume were observed in monosodium urate crystal-induced mice. However, upon treatment with 6-Gingerol, these biochemical alterations were brought back to near normal levels as comparable to indomethacin treatment. 6-Gingerol also reduced the acid phosphate and lactate dehydrogenase release in monosodium urate crystal incubated PMNL cells in vitro. These results strongly support the possibility of 6-Gingerol to be employed as an anti-inflammatory agent against gouty arthritis.

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6-Gingerol, an active ingredient of ginger suppresses monosodium ureate crystal-induced inflammation: An in vivo and in vitro evaluation

MiR-145-5p mitigates dysregulated Wnt1/β-catenin signaling pathway in rheumatoid arthritis.

Mangiferin is a natural polyphenolic (C-glucoxyl xanthone) antioxidant present in the bark, fruits, roots and leaves of Mangifera indica Linn. In the present study, we investigated the protective effect of mangiferin against carbon tetrachloride (CCl4)-induced hepatotoxicity in mice and compared it with silymarin, a standard hepatoprotective drug. The pretreatment of mangiferin (30 mg/kg body weight, i.p.) has shown it to possess a significant protective effect by lowering the serum aspartate and alanine aminotransferases, alkaline phosphatase, bilirubin and inflammatory mediator TNF-α. This hepatoprotective action was confirmed by histological observation. In addition, pretreatment of mangiferin prevented the elevation of hepatic malondialdehyde formation and the depletion of antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and total reduced glutathione) activity in the liver of CCl4-injected mice. The results suggest that mangiferin exhibits potent hepatoprotective effects on CCl4-induced liver damages in mice.

Mangiferin, a natural polyphenol protects the hepatic damage in mice caused by CCl4 intoxication

In the present study, the purpose was to investigate the effect of p-coumaric acid on the mRNA-expression levels of inflammatory cytokines, transcription factor, MAP kinases, and apoptotic proteins by real time reverse transcription polymerase chain reaction in the cardiac tissue of sodium arsenite exposed rats. Sodium arsenite administration (5 mg/kg/b.wt, once daily for 30 days) upregulated the mRNA-expression levels of inflammatory cytokines (interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and tumor growth factor-beta), transcription factor (NF-Kb-Rel A), protein kinases (Janus kinase and p38), caspase 3, and proapoptotic protein Bax in the cardiac tissue of rats, but the antiapoptotic protein Bcl-2 mRNA expression was found be downregulated. However, p-coumaric acid (75, 100 mg/kg/b. wt. oral) pretreatment daily before the sodium arsenite exposure protected the changes in the above mRNA-expression profiles observed in the cardiac tissues. In conclusion, this study confirmed that p-coumaric acid could be a promising dietary agent for protecting against the sodium arsenite-induced cardiotoxicity.

Mahaboobkhan Rasool

Papers

PdCl 2 -catalyzed synthesis of a new class of isocoumarin derivatives containing aminosulfonyl / aminocarboxamide moiety: First identification of a isocoumarin based PDE4 inhibitor.

6-Gingerol, an active ingredient of ginger suppresses monosodium ureate crystal-induced inflammation: An in vivo and in vitro evaluation

MiR-145-5p mitigates dysregulated Wnt1/β-catenin signaling pathway in rheumatoid arthritis.

Mangiferin, a natural polyphenol protects the hepatic damage in mice caused by CCl4 intoxication

Modulation of gene-expression profiles associated with sodium arsenite-induced cardiotoxicity by p-coumaric acid, a common dietary polyphenol.