Antioxidant potential of bitter cumin (Centratherum anthelminticum (L.) Kuntze) seeds in in vitro models

<p>Abstract</p> <p>Background</p> <p>Bitter cumin (<it>Centratherum anthelminticum </it>(L.) Kuntze), is a medicinally important plant. Earlier, we have reported phenolic compounds, antioxidant, and anti-hyperglycemic, antimicrobial activity of bitter cumin. In this study we have further characterized the antioxidative activity of bitter cumin extracts in various in vitro models.</p> <p>Methods</p> <p>Bitter cumin seeds were extracted with a combination of acetone, methanol and water. The antioxidant activity of bitter cumin extracts were characterized in various <it>in vitro </it>model systems such as DPPH radical, ABTS radical scavenging, reducing power, oxidation of liposomes and oxidative damage to DNA.</p> <p>Results</p> <p>The phenolic extracts of bitter cumin at microgram concentration showed significant scavenging of DPPH and ABTS radicals, reduced phosphomolybdenum (Mo(VI) to Mo(V)), ferricyanide Fe(III) to Fe(II), inhibited liposomes oxidation and hydroxyl radical induced damage to prokaryotic genomic DNA. The results showed a direct correlation between phenolic acid content and antioxidant activity.</p> <p>Conclusion</p> <p>Bitter cumin is a good source of natural antioxidants.</p

Ascorbyl esters for the treatment of cancer

There is provided a method of treating cancer by treating the cancer cells with a lipophilic derivative of ascorbic acid. Also provided is a method of inhibiting the Ras pathway by administering a lipophilic derivative of ascorbic acid. A method of inducing apoptosis in cancer cells is also provided by treating cancer cells with a lipophilic derivative of ascorbic acid. A pharmaceutical composition for the treatment of cancer comprising a lipophilic derivative of ascorbic acid in a pharmaceutically acceptable carrier is also provided

Epinephrine Increases Spinal Cord Concentrations of [(3) H]-Clonidine Hydrochloride in Rabbits After Epidural Infusion

Epinephrine is often given with epidurally administered drugs to prolong and enhance analgesia, which is partly attributed to alpha-adrenergic processes. This investigation evaluates the effect of epinephrine on the distribution of epidurally administered [() H]-clonidine hydrochloride (clonidine HCl) in serum and in the central nervous system. After placing a lumbar epidural catheter via a laminectomy, rabbits were randomly assigned to receive 20 micro Ci of clonidine HCl with epinephrine (1:200,000) (n = 5) or without (control; n = 5) for 90 min. During the administration, which included bolus and slow infusion, blood samples were collected at 15-min intervals. At the end of the administration, rabbits were perfused with normal saline, leading to exsanguination. Brain and spinal cord tissues were excised for radiometric analysis. In both groups, the concentration of clonidine HCl was greatest in the lumbar cord. Epinephrine further enhanced accumulation of clonidine HCl into the lumbar cord but did not alter the concentration of clonidine HCl in serum, brain, cervical cord, and thoracic cord. We conclude that lumbar administration of epidural clonidine HCl leads to increased concentrations in the lumbar cord, which is further enhanced by epinephrine. The increased spinal cord accumulation of clonidine may be another mechanism by which epinephrine improves epidural analgesia.(Anesth Analg 1997;85:324-7

The therapeutic effects of epidural intercellular adhesion molecule-1 monoclonal antibody in a rabbit model: involvement of the intercellular adhesion molecule-1 pathway in spinal cord ischemia

The pathophysiology of ischemia/reperfusion injury involves extravascular migration of leukocytes from the bloodstream to the site of injury. Leukocyte adhesion and intercellular adhesion molecule-1 (ICAM-1) play an important role in the recruitment of leukocytes to the site of injury. In this study, we evaluated the role of the ICAM-1 in spinal cord ischemia and the therapeutic effects of epidural ICAM-1 monoclonal antibody (Mab). The descending aorta was occluded below the renal artery with an aneurysm clip in rabbits anesthetized with halothane. The following variables were evaluated, in addition to ICAM-1 expression in the lumbar spinal cord, in animals receiving saline or ICAM-1 Mab via the epidural route: (1) leukocyte recruitment in the lumen of capillary vessels of the lumbar spinal cord (L6-7) at 8 h after 30 min of aortic occlusion and (2) neurological evaluation at 20 h after aortic occlusion of 10, 15, 17.5, 20, or 25 min. Paraplegia was graded with the following scale: Grade 0, no deficit; Grade 1, partial deficit; and Grade 2, complete paraplegia. Spinal cord ischemia increased the expression of ICAM-1 in the endothelium of spinal cord capillaries and led to capillary leukocyte recruitment and extravascular migration into the lumbar spinal cord parenchyma, which was ablated with epidural ICAM-1 Mab. Epidural ICAM-1 Mab reduced neurological deficits and offered neuroprotection. These findings demonstrate the involvement of the ICAM-1 pathway in spinal cord ischemia and the neuroprotective effects of epidural ICAM-1 Mab. Strategies to ameliorate spinal cord ischemia may entail the administration of leukocyte antiadhesion molecules into the neuraxial space

Clinical predictors of arterial extravasation, rebleeding and mortality following angiographic interventions in gastrointestinal bleeding

The aim of this study was to identify clinical and imaging predictors of arterial extravasation, post embolization rebleeding and 30-day mortality in gastrointestinal (GI) bleeding.This retrospective study included 114 patients who underwent angiography for upper or lower GI bleeding. Multivariate logistic regression was used to identify clinical and imaging predictors.Angiography demonstrated arterial extravasation in 22 patients (19%) and embolization was performed in 48 (42%) patients including prophylactic embolization in 26 (56%). Fall in hemoglobin level from baseline was an independent predictor of arterial extravasation with 65% increased odds for every unit drop (OR 1.65, 95%CI 1.13-2.40, p=0.01). Age <60 years was a negative predictor of rebleed within 30-days (OR 0.94, 95%CI 0.89-1.00, p=0.04). Patients with a history of malignancy were more likely to rebleed (OR 4.4, 95%CI 1.06-18.36, p=0.04). Hemodynamic instability prior to angiography (OR 13.22, 95%CI 1.65-106.07, p=0.02), history of malignancy (OR 1.36, 95%CI 1.49-10.49, p=0.01), number of units of platelets transfused (OR 1.42, 95%CI 1.02-1.97, p=0.04) and rebleed after angiography (OR 46.8, 95%CI 4.80-456.14, p<0.01) were predictors of 30-day mortality. Prophylactic embolization was not a predictor of rebleed or 30-day mortality.This paper identified important clinical predictors of arterial extravasation, rebleed and 30-day mortality in GI bleedings, which will assist in patient selection and help to improve the overall angiographic management of GI bleeding