Showing 9 results for Kadkhodaee
M Kadkhodaee , A Poosti , F Shahbazi , H Farmand , M Jorjany ,
Volume 57, Issue 3 (8 1999)
Abstract
Indacrinone is a loop diuretic which also has uricosuric, kaliuretic, saliuretic and natriuretic effects. Since it has been reported that this drug has several actions in different organs, we decided to evaluate its mechanism of action on the rat jejunum smooth muscle. After preparation of the tissues, different concentrations of indacrinone were applied. Doses of 8.2×10^-6 M, 2.7×10^-5 M, 8.2×10^-5 M and 2.7×10^-4 M were all effective in a dose dependent manner to relax the muscle. Increase in the drug concentration resulted in much faster reduction in twitch amplitude. The jejunum is innervated by adernergic, cholinergic, serotonergic and histaminergic systems. To find the mechanism of action of indacrinone in rat jejunum, experiments were conducted by appropriate receptor agonists and antagonists of the above systems. There was a marked increase in muscle contraction tone and ampliture by the use of histamine, while indacrinone prevented the increase induced by histamine. It was concluded that indacrinone may be a competitive antagonist for histamin receptors in rat jejunum muscle.
R. Ghaznavi, M. Kadkhodaee, H. Khastar, M.zahmatkesh,
Volume 64, Issue 5 (1 2006)
Abstract
Background: In recent publications, several mechanisms have been implicated in gentamicin (GM) nephrotoxicity. Reactive oxygen species have been proposed as one of the causative factors of the drug renal side effects. This study was designed to evaluate the protective effects of the antioxidant vitamins against GM-mediated nephropathy in insitu isolated rat kidneys.
Methods: Male Sprague-Dawley rats were randomly assigned to one of the following groups of seven rats: Group 1 (control) was tyrode perfused kidneys. Group 2 (GM), 200µg/ml gentamicin was added to the perfusate. Group 3 (GM + Vit C), the same as group 2 but vitamin C (200 mg/L) was added to the drinking water for 3 days and 100 mg/L to the perfusate. Group 4 (GM + Vit E), the same as group 2 but vitamin E (100 mg/100 g BW, ip) was injected 12 h before experiments. Group 5 (GM + Vit C + Vit E) the same as group 2 but Vit E and C were co-administered (same as Group 3 & 4). Urinary N-acetyle-B-D-glucosaminidas (NAG) and renal cortex superoxide dismutase (SOD) levels were measured and tissue histological evaluations were performed.
Results: Gentamicin caused a significant nephrotoxicity demonstrated by increase in urinary NAG. Decline in SOD contents were observed comparing to controls. Vit C or Vit E inhibited the gentamicin-induced increased releases of NAG into urine but did not show a significant effect on the SOD levels.
Conclusion: Co-administration of VitC&E significantly prevented the GM nephrotoxicity demonstrating by preservation of SOD levels and prevention of increase in urinary enzyme activities. Histological studies of renal tissues provided additional evidences for protective effects of antioxidant vitamins. We concluded that moderate doses of Vit C & E have protective effects in gentamicin nephrotoxicity and co-administration of these vitamins have additional beneficial effects.
Hemmati M, Kadkhodaee M, Zahmatkesh M, Mahdavi-Mazde M, Ghaznavi R, Mirershadi F,
Volume 66, Issue 1 (30 2008)
Abstract
Background: The risk of atherosclerosis and cancer is high in hemodialysis (HD) patients. There is evidence that HD causes oxidative stress. However, the causative factors of oxidative stress are unknown. It has been suggested that HD imposes an additional oxidative stress on patients with chronic renal failure by activation of granulocytes on dialyzer membranes resulting in an imbalance between oxidants and antioxidants. In this regard, a number of reports, either measuring specific analytes or enzymes, or estimating the total antioxidant activity of the plasma have given contradictory and inconclusive results. To investigate the oxidative stress status in Iranian HD patients, in this study, we evaluated GSH and FRAP levels along with Ca and pH in the blood of these patients.
Methods: Along with 20 healthy age and gender matched control subjects, 24 patients underwent dialysis, three times per week, for four hours in each session. Before and after dialysis, blood was taken for biochemical and liver function tests and to evaluate oxidative stress markers and measure Ca and pH levels.
Results: There was a significant decrease in FRAP and GSH levels after dialysis compared to those before treatment. Dialysis caused an increase in pH and Ca levels compared to levels in control subjects after dialysis.
Conclusion: In general, before dialysis, there is a balance between oxidants and antioxidants however, due to higher levels of oxidants as well as the possible binding of antioxidants to the dialyzer membrane during dialysis, an imbalance occurs. The instability in the balance of oxidants and antioxidants may be the major cause of cellular oxidative damage found in HD patients. This study indicates that there is a significant level of oxidative stress in renal chronic patients and this stress is augmented by dialysis. Antioxidant therapy should be considered in these patients.
Kadkhodaee M, Golab F, Zahmatkesh M, Ghaznavi R, Hedayati M, Arab Ha, Soleimani M,
Volume 67, Issue 7 (7 2009)
Abstract
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Background: The effect of ischemia/reperfusion (I/R) injury on kidney has
been under investigation for many years. But the changes in liver function and
oxidative stress status in renal I/R injury is not well known. Recent studies
suggest a crosstalk between liver and kidneys. The aim of the present study was
to assess liver changes after induction of various degrees of renal I/R injury.
Methods: This is an
experimental study conducted on 20
male rats that were obtained from animal house of Physiology Department. Twenty
male rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion
periods. Blood samples were drawn post-operatively and plasma creatinine, BUN, ALT and AST were measured.
Hepatic glutathione (GSH) and FRAP (ferric reducing antioxidant power) levels and the concentration
of IL-10 and tumor necrosis
factor (TNF) -alpha were
evaluated.
Results: Both 45 and 60 min ischemia
followed by 1h reperfusion periods
resulted in significant increases in plasma creatinine (11.1±1.7mg/dl and 1.24±0.07mg/dl vs 0.55±0.15mg/dl, p<0.05) and BUN (34±3.85mg/dl and 35.0±2.81mg/dl vs 23.75±1.1mg/dl, p<0.05). These rats
showed a significant decrease in liver GSH as well as significant increase in TNF-a & IL-10 concentrations.
Conclusion: Renal ischemia causes
changes in liver function and oxidative stress status. A minimum of 45 min ischemia is needed to
study the effects of renal injury on liver as a remote affected organ.
Kadkhodaee M, Khastar H, Seifi B, Najafi A, Delavari F,
Volume 70, Issue 2 (4 2012)
Abstract
Background: In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR (60 min of bilateral renal artery occlusion and 3 hrs reperfusion) injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors.
Methods: Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group (Sham recipient) and the intact recipient mice that received leukocytes from IR donor group (IR recipient). After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected.
Results: Renal malondialdehyde (MDA) increased and glutathione and superoxide dismutase (SOD) decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group.
Conclusion: These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury.
Atefeh Mahmoudi , Mehri Kadkhodaee , Fereshteh Golab , Atefeh Najafi , Zahra Sedaghat , Parisa Ahghari ,
Volume 71, Issue 8 (November 2013)
Abstract
Background: Several studies indicate that gender differences exist in tolerance of the kidney to ischemia reperfusion (IR) injury. Recently, postconditioning (POC), induction of brief repetitive periods of IR, has been introduced to reduce the extent of the damage to the kidney. This method was shown to attenuate renal IR injury by modifying oxidative stress and reducing lipid peroxidation. Considering the gender effect on the results of several treatment methods, in this study, we investigated the impact of gender on the protective effect of POC on the rat kidney.
Methods: In this study, after right nephrectomy, 48 male and female rats were randomly divided into 6 groups of 8 rats: In IR group, with the use of bulldog clamp, 45 minutes of left renal artery ischemia was induced followed by 24 hours of reperfusion. In the sham group, all of the above surgical procedures were applied except that IR was not induced. In the POC group, after the induction of 45 minutes ischemia, 4 cycles of 10 seconds of intermittent ischemia and reperfusion were applied before restoring of blood to the kidney. 24 hours later, serum and renal tissue samples were collected for renal functional monitoring and oxidative stress evaluation.
Results: Postconditioning attenuated renal dysfunction considering the significant decrease in plasma creatinine and BUN compared with IR group only in male rats (P<0.05). Also, POC attenuated oxidative stress in male rats’ kidney tissues as demonstrated by a significantly reduced malondialdehyde (MDA) level and increased superoxide dismutase (SOD) activity (P<0.05). In female rats, there were no changes in functional markers and oxidative stress status in POC group compared to IR group.
Conclusion: Considering gender difference, POC had protective effect against IR injury by attenuating functional and oxidative stress markers in male rat kidneys. This protective effect was not seen in female rats.
Behjat Seifi, Mehri Kadkhodaee , Enayatollah Bakhshi, Mina Ranjbaran , Parisa Ahghari , Bahareh Yasrebi ,
Volume 72, Issue 2 (May 2014)
Abstract
Background: The renal sympathetic nerve activity (RSNA) is enhanced in renal failure. Paraventricular nucleus in hypothalamus is an important central site to regulate sympathetic activity. There are angiotensin II (Ang) II receptors in this nucleus. The aim of this study was to evaluate the effects of angiotensin II in hypothalamic paraventricular nucleus (PVN) on renal ischemia-reperfusion injury and RSNA.
Methods: This study was done at 2013 in Physiology department of Tehran University of Medical Sciences. One week before the induction of renal Ischemia-Reperfusion (IR) in Sprague-Dawley rats, a cannula was inserted into the right PVN for microinjection of different doses of Ang II (3, 30, and 300 ng). Then right nephrectomy was done. After one week recovery, renal IR injury was induced by clamping the left renal artery for 45 minute and then reperfusion for 3 or 24 hour. Ten minutes before the induction of renal ischemia-reperfusion, administration of different doses of angiotensin II were done in different groups. In all animals, left renal sympathetic activity was recorded before and during renal ischemia. After 3 or 24 hours reperfusion the blood, kidney and brain were collected to assay renal function and histology and oxidative stress indices Superoxide Dismutase, SOD and Malondialdehyde, MDA) in PVN.
Results: Administration of different pharmacological doses of angiotensin II into PVN exaggerated the renal IR injury. Angiotensin II in different doses increased the plasma creatinine and BUN levels and renal histological markers in comparison to renal IR in-jury (P<0.05). Angiotensin II had detrimental effects on RSNA and oxidative stress in-dices Super Oxide Dismutase (SOD) and Malondialdehyde (MDA) in PVN as the dose was increased (P<0.05).
Conclusion: These data showed that the PVN is a responsive site for central Ang II-induced damage in renal IR injury. We suggested the central effects of Ang II in the PVN on renal IR injury are mediated by oxidative stress in the PVN, and the peripheral effects by a sympathetic pathway.
Fateme Azizi , Behjat Seifi , Mehri Kadkhodaee ,
Volume 75, Issue 9 (December 2017)
Abstract
Background: Renal ischemia reperfusion (RIR) injury is a common clinical syndrome that affects renal function and significantly increases morbidity and mortality. Hydrogen sulfide (H2S) is an endogenously gaseous mediator that exhibits many cytoprotective effects. Recently, studies have shown that H2S have opposite effects in different doses. Therefore, in the current study we investigated the effects of H2S at different doses on renal function after induced renal ischemia reperfusion injury model.
Methods: The present study is an experimental study in animals and was conducted in Tehran University of Medical Sciences in April 2014. Male Wistar rats were assigned to five main groups (n= 6): 1) Sham, 2) Ischemia reperfusion (IR), 3) Administration of 50 µmol/kg Sodium hydrosulfide (NaHS)+IR, 4) Administration of 75 µmol/kg NaHS+IR and 5) Administration of 125 µmol/kg NaHS+IR. Sham group underwent laparotomy without cross-clamping of renal pedicles. Renal ischemia (IR) was induced in rats by both renal arteries occlusion for 55 min followed by reperfusion. Rats in the NaHS groups received intraperitoneal injections of 50, 75, or 125 µmol/kg of NaHS 10 minutes before the onset of ischemia and immediately after the onset of reperfusion. After reperfusion, plasma was collected for functional evaluation.
Results: Compared to the sham, IR animals demonstrated a significant rise in plasma creatinine and BUN levels. Rats in the low-dose NaHS treated groups (H50, H75) had improved renal function by significantly decrease of creatinine and BUN levels. However, treatment with a high-dose of NaHS increased the levels of plasma creatinine and BUN levels as compared with these indices in the IR group.
Conclusion: Our study demonstrates that different doses of Sodium hydrosulfide (NaHS) can play diverse role in renal ischemia reperfusion injury. However, NaHS in the low-doses could protect the kidney from the RIR injury, in a higher dose NaHS exaggerated the renal function by increases plasma creatinine and BUN. Therefore, determining of the therapeutic doses of NaHS may be important in the protection of kidney from the RIR injury.
Farzaneh Kianian, Mehri Kadkhodaee, Behjat Seifi, Fariba Akhondzadeh, Kamal Abdolmohammadi , Arash Abdi, Mina Ranjbaran,
Volume 79, Issue 8 (November 2021)
Abstract
Background: In the present study, we hypothesized that conditioned medium (CM) derived from mesenchymal stem cells attenuates the brain oxidative stress in sepsis induced by the cecal ligation and puncture (CLP) model.
Methods: This study was performed in the Department of Physiology at Tehran University of Medical Sciences from August 2018 to April 2019. Conditioned medium was collected from mesenchymal stem cells isolated from rat's adipose tissues at the second culture passage. Male Wistar rats weighting (220-250 g) were randomly divided into three experimental groups (n=8 each): Sham, Sepsis and CM. Sepsis was induced by cecal ligation and puncture model in the Sepsis and CM groups. Animals in the CM group received the conditioned medium from 5×10
5 mesenchymal stem cells (2 h after sepsis induction, i. p., 3-5 mL). The systolic blood pressure and O2 saturation were measured 24 h after the treatment. The plasma and brain tissue samples were taken for inflammatory and oxidative stress assessment, respectively.
Results: Septic rats showed a significantly lower systolic blood pressure and O2 saturation level. They also had a significant increase in the plasma inflammatory indices (tumor necrosis factor-alpha [TNF-α], interleukin-6 [IL-6]) and brain malondialdehyde (MDA) content as well as a significant reduction in the brain superoxide dismutase (SOD) activity compared to the Sham group. The CM group had significantly higher systolic blood pressure and O2 saturation level compared to the septic rats. The animals in the CM group showed a significant attenuation in the plasma inflammatory indices (TNF-α and IL-6) and brain MDA content while having a significantly higher brain SOD activity compared to the Sepsis group.
Conclusion: Our findings showed that conditioned medium derived from mesenchymal stem cells has protective effects in preventing the inflammatory and oxidative stress status and may be suggested as a promising treatment in patients suffering from sepsis and septic shock. |
