Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

http://academic.oup.com/milmed/article-pdf/146/7/506/24126715/milmed-146-7-506.pdf

Goodman and Gilman's The Pharmacological Basis of Therapeutics

Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues.

/pdf/cell-biology-of-ischemia-reperfusion-injury-1rdtb8k8os.pdf

Cell Biology of Ischemia/Reperfusion Injury

The incidence rate of AKI in hospitalized patients is increasing. However, relatively little attention has been paid to the association of AKI with long-term risk of adverse coronary events. Our study investigated hospitalized patients who recovered from de novo dialysis-requiring AKI between 1999 and 2008 using patient data collected from inpatient claims from Taiwan National Health Insurance. We used Cox regression with time-varying covariates to adjust for subsequent CKD and ESRD after discharge. Results were further validated by analysis of a prospectively constructed database. Among 17,106 acute dialysis patients who were discharged, 4869 patients recovered from dialysis-requiring AKI (AKI recovery group) and were matched with 4869 patients without AKI (non-AKI group). The incidence rates of coronary events were 19.8 and 10.3 per 1000 person-years in the AKI recovery and non-AKI groups, respectively. AKI recovery associated with higher risk of coronary events (hazard ratio [HR], 1.67; 95% confidence interval [95% CI], 1.36 to 2.04) and all-cause mortality (HR, 1.67; 95% CI, 1.57 to 1.79) independent of the effects of subsequent progression to CKD and ESRD. The risk levels of de novo coronary events after hospital discharge were similar in patients with diabetes alone and patients with AKI alone (P=0.23). Our results reveal that AKI with recovery associated with higher long-term risks of coronary events and death in this cohort, suggesting that AKI may identify patients with high risk of future coronary events. Enhanced postdischarge follow-up of renal function of patients who have recovered from temporary dialysis may be warranted.

Long-Term Risk of Coronary Events after AKI

http://if-pan.krakow.pl/pjp/pdf/2012/1_31.pdf

Animal models of acute renal failure

/pdf/cardioprotective-effect-of-rutin-considering-cardiac-enzyme-4s82bevhh4.pdf

Cardioprotective effect of rutin considering cardiac enzyme level in induced myocardial infarction

Diabetes Type-II Exaggerates Renal Ischemia Reperfusion Injury by Elevation of Oxidative Stress and Infl ammatory Response

Parkinson’s disease is progressive neurodegenerative disease that occurs due to several causative factors although dopamine deficiency is prime characteristic of the disease. Environmental toxin, genetic abnormalities, drugs, oxidative stress are some of causative factor responsible for development of parkinson’s disease. Current pharmacotherapy of this disorder is able to provide only sy mptomatic relief. Moreover their use is associated with lot of adverse effects. The importance of medicinal plants comes in this context. In present study oxotremorine (2 mg/kg) was used to induce the parkinsonism in wistar albino rats. Hydroalcoholic extr acts of Parkinsonia aculeata L. seeds at the dose of (200 mg/kg) and Ananas cosmosus L. Fruits at the dose (250 mg/kg) were administered. The extracts of both the plants were administered prior to oxotremorine administration. At the interval of each hour t remor score, rigidity score, hypokinesia score, postural flexion score and postural immobility score were recorded. The result data shows that oxotremorine induces the tremor, rigidity, hypokinesia, postural flexion and postural immobility where as adminis tration of hydroalcoholic extracts of Parkinsonia aculeata L. seeds at the dose of (200 mg/kg) and Ananas cosmosus L. fruits at the dose (250 mg/kg) significantly reduced the tremor score, rigidity score, hypokinesia score, postural flexion and postural im mobility score at (P < 0.05).

/pdf/effect-of-hydroalcoholic-extracts-of-parkinsonia-aculeata-l-1gm0ylgfpp.pdf

Effect of hydroalcoholic extracts of parkinsonia aculeata l. and ananus comosus l. on oxotremorine induced parkinsonism in wistar a lbino rats

Parkinson ’s disease is c ommon hypo kinetic disorder mainly occurs by the neurodegener ation in central nervous system affecting the 2 - 3% of population all over the world above age 60 years. Major symptoms are tremor , rigidity , bradykinesia and posture instability. There are predis posing factor like metal exposure, family history, extreme stress and head trauma that promote the progression of Parkinson’s disease. Other risk factors includes the advanced age, environmental toxins, oxidative stress, inflammation, viral infections and intake of several dopamine antagonists play a contributory role in development of Parkinson ’s disease . The Parkinson’s disease occurs due to a reduction in the striatal dopamine content in excess of 80%. The primary area of neurodegeneration in PD is the l oss of dopaminergic neurons in the Substantia nigra par - compacta. Several proteins like α - synculine, ubiquitine - carboxy hydrolase terminal - 1, PINK1 and DJ - 1 are involved in the formation of lewis bodies which is hall mark of pathogenesis of Parkinson’s dis ease. Currently dopamine agonist, Monoamine oxidase A, B inhibitors are widely used for the treatment of Parkinson ’s disease, although it bears the risk of adverse reaction . Now a day the medicinal plants which are less toxic and more preferred over the co nventional therapeutics. In this review we have focus on pathophy s iology, risk factors and possible traditional medicine useful for retarding the progression of Parkinson’s disease.

Parkinson 's disease: a review on etio patho genesis and herbal therapy

/pdf/parkinson-s-disease-a-review-on-etiopathogenesis-and-herbal-572a2yry53.pdf

N. P. Jivani

Papers

Cardioprotective effect of rutin considering cardiac enzyme level in induced myocardial infarction

Diabetes Type-II Exaggerates Renal Ischemia Reperfusion Injury by Elevation of Oxidative Stress and Infl ammatory Response

Effect of hydroalcoholic extracts of parkinsonia aculeata l. and ananus comosus l. on oxotremorine induced parkinsonism in wistar a lbino rats

Parkinson 's disease: a review on etio patho genesis and herbal therapy

Parkinson’s disease: a review on etiopathogenesis and herbal therapy