Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam.

OBJECTIVE: We tested the hypothesis that postpartum combined oral contraceptive (COC) treatment would induce oxidative stress via the adenosine deaminase-xanthine oxidase pathway in the kidney. We also sought to determine whether mineralocorticoid receptor (MR) or glucocorticoid receptor (GR ) blockade would suppress the activities of ADA and xanthine oxidase caused by postpartum COC treatment in the kidney. METHODS: Twenty-four Wistar dams were randomly assigned to 4 groups (n = 6/group). Dams received vehicle (po), COC (1.0 µg ethinylestradiol and 5.0 µg levonorgestrel; po), COC with GR blockade (mifepristone; 80.0 mg/kg; po), and COC with MR blockade (spironolactone; 0.25 mg/kg; po) daily between 3rd and 11th week postpartum. RESULTS: Data showed that postpartum COC caused increased plasma creatinine and urea, increased renal triglyceride/high-density lipoprotein ratio, free fatty acid accumulation, alanine aminotransferase, gamma-glutamyltransferase, uric acid, and activities of renal XO and ADA. On the other hand, postpartum COC resulted in decreased plasma albumin, renal glutathione, and Na+-K+-ATPase activity with no effect on lactate production. However, MR or GR blockade ameliorated the alterations induced by postpartum COC treatment. The present results demonstrate that MR or GR blockade ameliorates postpartum COC-induced increased activities of ADA and xanthine oxidase and restores glutathione-dependent antioxidative defense. CONCLUSION: These findings implicate the involvements of GR and MR in renal dysfunctions caused by COC in dams via disrupted glutathione antioxidative barrier.

Report on a Double Phrygian Cap and Phrygian prominence in a Nigerian population

It is debatable among anatomists whether the Phrygian cap of the gall bladder is an anomaly or anatomic variation with an incidence of 4.0% reported. A 2-fold increase of 7.9% during a 5-year population study was observed in Lagos, Nigeria. A 48-year old male with minimal (non-acute) epigastric discomfort was referred for ultrasound after suspicious cholecystitis. On radiological evaluation, a double "Phrygian cap" was found by coincidence. There is no recent emphasis on double Phrygian cap study, thus it is reported for its rarity and difficulty in arriving at conclusive diagnosis. Common imaging choice is mostly by multi-slice CT for biliary aspects and appendages. Most Phrygian caps are asymptomatic with little or no pathologic consequence. Surgical intervention (cholecystectomy) for a Phrygian cap is only indicated in case of recurrent symptoms. To our knowledge, sparse anatomic and ultrasound literature exists on the Phrygian cap, thus the need for this rare case report

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Sodium azide-induced degenerative changes in the dorsolateral prefrontal cortex of rats: attenuatingmechanisms of kolaviron

Identification of therapeutic targets following neurodegeneration is of major biomedical importance. Kolaviron (Kv) is a biflavonoid complex isolated from seeds of Garcina kola - a common oral masticatory agent in Nigeria known to hold medicinal value. Therefore this study evaluated the therapeutic potential of Kv on cells of the dorsolateral prefrontal cortex (DLPFC), before or after sodium azide (NaN3)-induced neurodegeneration. Rats were randomly assigned into 5 groups (6 each) and treated daily (orally) as follows: 1 ml of corn-oil (vehicle of Kv, 21 days); Kv only (200 mg/kg) for 21 days; NaN3 only (20 mg/kg for 5 days); NaN3 (20 mg/kg for 5 days) followed by Kv (200 mg/kg for 21 days); Kv (200 mg/kg for 21 days) followed by NaN3 (20 mg/kg for 5 days). After treatments, rats were sacrificed and perfused transcardially (with 4% PFA) with brains fixed in accordance with the technique to be used. The DLPFC was examined using histology (H&E), immunoperoxidase (GFAP), immunofluorescence (iNOS & nNOS) and Western blotting (MAPT, MAP2, Bax, BCL-2 and CAD). Quantitative analysis was done using ImageJ software and statistical analysis with Graphpad prism (ANOVA) at p<0.05. NaN3 treatment induced neuronal damage, characterized by reduced relative brain weight, pyknosis, karyorrhesis, astrogliosis, axonal/dendritic damage and cytoskeletal dysregualtion that subsequently resulted in increased expressions of apoptotic regulatory proteins. These degenerative changes were relatable to the observed iNOS and nNOS upregulations. However, Kv administration attenuated the NaN3- initiated destructive molecular cascades in the DLPFC of rats through mechanisms that involved inhibition of stressor molecules and toxic proteins, prevention of stress related biochemical redox, preservation of neuronal integrity, cytoskeletal framework and subsequently, reduced the level of apoptotic regulatory proteins. We conclude that Kv conferred therapeutic benefits on NaN3- induced neurodegeneration, particularly when administered before more than after the insult

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Kolaviron was protective against sodium azide (NaN3) induced oxidative stress in the prefrontal cortex.

Kolaviron is a phytochemical isolated from Garcina kola (G. kola); a common oral masticatory agent in Nigeria (West Africa). It is a bioflavonoid used--as an antiviral, anti-inflammatory and antioxidant--in relieving the symptoms of several diseases and infections. In this study we have evaluated the neuroprotective and regenerative effect of kolaviron in neurons of the prefrontal cortex (Pfc) before or after exposure to sodium azide (NaN3) induced oxidative stress. Separate groups of animals were treated as follows; kolaviron (200 mg/Kg) for 21 days; kolaviron (200 mg/Kg for 21 days) followed by NaN3 treatment (20 mg/Kg for 5 days); NaN3 treatment (20 mg/Kg for 5 days) followed by kolaviron (200 mg/Kg for 21 days); 1 ml of corn-oil (21 days-vehicle); NaN3 treatment (20 mg/Kg for 5 days). Exploratory activity associated with Pfc function was assessed in the open field test (OFT) following which the microscopic anatomy of the prefrontal cortex was examined in histology (Haematoxylin and Eosin) and antigen retrieval Immunohistochemistry to show astroglia activation (GFAP), neuronal metabolism (NSE), cytoskeleton (NF) and cell cycle dysregulation (p53). Subsequently, we quantified the level of Glucose-6-phosphate dehydrogenase (G6PDH) and lactate dehydrogenase (LDH) in the brain tissue homogenate as a measure of stress-related glucose metabolism. Kolaviron (Kv) and Kolaviron/NaN3 treatment caused no prominent change in astroglia density and size while NaN3 and NaN3/Kv induced astroglia activation and scar formation (astrogliosis) in the Pfc when compared with the control. Similarly, Kolaviron and Kv/NaN3 did not alter NSE expression (glucose metabolism) while NaN3 and NaN3/Kv treatment increased cortical NSE expression; thus indicating stress related metabolism. Further studies on enzymes of glucose metabolism (G6PDH and LDH) showed that NaN3 increased LDH while kolaviron reduced LDH in the brain tissue homogenate (P < 0.001). In addition kolaviron treatment before (P < 0.001) or after (P < 0.05) NaN3 treatment also reduced LDH expression; thus supporting its role in suppression of oxidative stress. Interestingly, NF deposition increased in the Pfc after kolaviron treatment while Kv/NaN3 showed no significant change in NF when compared with the control. In furtherance, NaN3 and NaN3/Kv caused a decrease in NF deposition (degeneration). Ultimately, the protective effect of KV administered prior to NaN3 treatment was confirmed through p53 expression; which was similar to the control. However, NaN3 and NaN3/Kv caused an increase in p53 expression in the Pfc neurons (cell cycle dysregulation). We conclude that kolaviron is not neurotoxic when used at 200 mg/Kg BW. Furthermore, 200 mg/Kg of kolaviron administered prior to NaN3 treatment (Kv/NaN3) was neuroprotective when compared with Kolaviron administered after NaN3 treatment (NaN3/Kv). Some of the observed effects of kolaviron administered before NaN3 treatment includes reduction of astroglia activation, absence of astroglia scars, antioxidation (reduced NSE and LDH), prevention of neurofilament loss and cell cycle regulation.