Pre‐medication and renal pre‐conditioning: a role for alprazolam, atropine, morphine and promethazine

Ajami, Marjan; Habibey, Rouhollah

doi:10.1111/j.1472-8206.2009.00743.x

Cited by 33 publications

(17 citation statements)

References 47 publications

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“…Atropine group animals were treated by an intraperitoneal (i.p.) injection of atropine at a dose of 15 mg/kg/day for 7 days; the control group animals were treated with normal saline for 7 days in equal volumes as for the experimental groups (15). After 7 days of treatment with atropine (15 mg/kg/day), the control and experimental animals were anesthetized with xylazine (10 mg/kg) and ketamine HCl (50 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Huang

Liu

2011

Mol Med Report

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Abstract. Atropine-induced heart damage is associated with changes in the expression of various enzymes and proteins. The purpose of this study was to investigate atropine-induced alterations in cardiac E-cadherin and 5-hydroxytryptamine (5-HT) after atropine administration. Male Wistar rats were randomly divided into two groups: a control group and an atropine group. The atropine group intraperitoneally received atropine at a single dose of 15 mg/kg for 7 days; the controls received the same amount of saline via the same route. On Day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and 5-HT. Sections were analyzed by digital image analysis. Cardiac protein expression of E-cadherin and 5-HT was altered after atropine-induced toxicity in the rat. The expression levels of E-cadherin and 5-HT were significantly decreased after atropine treatment, supported by IOD analysis, when compared with the control (P<0.05). The current findings indicate that such changes would be reflected in abnormal cardiac function, and these proteins may be useful for revealing the mechanisms underlying atropine-induced toxicity and may also provide various clues for further research.

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Section: Methodsmentioning

confidence: 99%

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Huang

Liu

2011

Mol Med Report

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“…Membranes were blocked with the blocking agent (BSA+ 0.05% Tween‐20) for overnight: then incubated with primary antibodies for 1 hr followed by a horseradish peroxidase‐conjugated secondary antibody (Anti‐rabbit IgG). Finally, protein detection was performed by Chemiluminescent HRP Substrate (Millipore) for 5 min and visualised on commercial x‐ray film (Pazoki‐Toroudi, Ajami, & Habibey, ; Pazoki‐Toroudi, Ajami, Babakoohi, et al., ).…”

Section: Methodsmentioning

confidence: 99%

FOXO1 targeting by capsaicin reduces tissue damage after testicular torsion

et al. 2018

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Testicular torsion-related oxidative stress causes a sequential chain of DNA damage, lipid peroxidation and cell death that leads to the derangement in the sperm functions and infertility. Capsaicin that has been applied for pain relief and cancer prevention possesses antioxidant properties which can be exploited to confer cell survival under ischaemic testis damage. Wistar male rats weighing 150-200 g were randomly divided into four groups: (i) sham group (all procedures except torsion of testis), (ii) ischaemia group (TT group), (iii) three TT groups treated with different dose of capsaicin (TT + different doses of Cap) and (iv) three control groups treated with different doses of capsaicin (100, 500 and 1000 ug/ml). Capsaicin administration significantly decreased the expression of pro-apoptotic factors and increased the expression of anti-apoptotic factors. Likewise, the expression of FOXO1 is significantly increased by higher doses of the capsaicin. Histological assessment by H&E and TUNEL method also exhibited an improved testicular morphology and decreased apoptosis in testes. These results suggested clinical potential for capsaicin in treatment of testicular torsion by targeting FOXO1 and apoptotic pathways.

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“…The method for determining the grade of damage to the renal tissue has been described previously [23]. All histological evaluations were done under an optical microscope.…”

Section: Histologymentioning

confidence: 99%

“…Three sections were prepared from each sample and then were evaluated by two pathologists unaware of the experimental groups and protocols. The method for determining the grade of damage to the renal tissue has been described previously [23]. Briefly, it was graded from 1 to 4 according to the following criteria: (0) for no sign of necrosis, (1) for necrosis of individual cells, (2) for necrosis of all cells in adjacent proximal convoluted tubules, with survival of surrounding (4) for necrosis affecting all the three segments of the proximal convoluted tubule.…”

Section: Histologymentioning

confidence: 99%

Effect of DHA+EPA on oxidative stress and apoptosis induced by ischemia‐reperfusion in rat kidneys

Ajami

Davoodi

Habibey

et al. 2012

Fundamemntal Clinical Pharma

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Apoptosis, as well as necrosis, has an important role in post-ischemic renal pathology. The effect of pretreatment with Docosahexaenoic acid+Eicosapentaenoic acid (DHA+EPA) on renal injury and apoptotic protein expression was evaluated. Right nephrectomy was completed on male Wistar rats (255-300 g). The rats received DHA+EPA (200 mg/kg/day) of distilled water orally for 14 days before ischemia reperfusion (IR) or sham operation. A total of 81 rats were divided into three main groups with 6, 24 and 48 h of post-operation or reperfusion period. Serum creatinine (SCr), BUN, creatinine clearance (CCr) and fractional excretion of sodium (FEN a ) were measured. Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities, Bax and Bcl-2 protein expressions and renal histological injury were determined. SCr, BUN and FEN a increased 6-48 h of reperfusion (P < 0.01). Tissue MDA content and Bax expression increased (P < 0.01) and CAT and SOD activities decreased (P < 0.05) in the IR group. DHA+EPA decreased SCr and BUN, FEN a , tissue MDA levels (P < 0.05 vs. IR) and increased CAT and SOD activities and Bcl-2 expression (P < 0.05 vs. IR) for 6-48 h after ischemia. IR induced mild (6 h, P < 0.05) and severe (24-48 h, P < 0.01) tissue damage. Mild-to-moderate tissue damage was observed in DHA+EPA groups from 6 to 48 h of reperfusion period (P < 0.05 vs. IR, 24-48 h). In conclusion, the results suggest that pre-ischemic exposure to DHA+EPA could improve the outcome of early graft function by inhibition of IR-induced oxidative stress and apoptosis.

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Pre‐medication and renal pre‐conditioning: a role for alprazolam, atropine, morphine and promethazine

Cited by 33 publications

References 47 publications

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

FOXO1 targeting by capsaicin reduces tissue damage after testicular torsion

Effect of DHA+EPA on oxidative stress and apoptosis induced by ischemia‐reperfusion in rat kidneys

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