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Articles by H.R. Khorram-Khorshid
Total Records ( 2 ) for H.R. Khorram-Khorshid
  Azadeh Mohammadirad , H.R. Khorram-Khorshid , Farhad Gharibdoost and Mohammad Abdollahi
  This review focuses on the efficacy of Setarud (IMOD) that is an effective new drug in the management of different conditions in animal and human. IMOD is a new natural mixture that demonstrated immune modulating activity in preliminary investigations. To conduct this review, all relevant databases were searched up to 20th August 2011 for the term IMOD or Setarud and all human, animal and in vitro studies considered the effects of IMOD. A total of 13 studies were included. Some human studies showed anti-inflammatory and anti-oxidative stress effects of IMOD by lowering tumor necrosis factor alpha (TNF-α) and CD4 (a glycoprotein expressed on the surface of T helper cells, monocytes, macrophages and dendritic cells) that are involved in process of inflammation and oxidative stress consequences. The positive effects of IMOD in the control of experimental models of colitis, diabetes, hyperchlosteromia, polycyctic ovary syndrome and liver injury were found that were mediated mainly through antioxidant and anti-inflammatory properties. IMOD has also enhanced secretion of insulin from the rat isolated pancreatic islets and human B lymphocyte. It is concluded that IMOD has optimistic effects on oxidative stress and pro-inflammatory conditions in various diseases which most probably is resulted from combinational effects of herbs and the elements present in the mixture of IMOD.
  H.R. Rahimi , M. Gholami , H.R. Khorram-Khorshid , F. Gharibdoost and M. Abdollahi
  Hepatoprotective effect and mechanisms of a novel selenium/electromagnetically treated multiherbal mixture named Setarud (IMODTM) in combination with silymarin (SM) a known hepatoprotective compound was investigated in acetaminophen-induced acute hepatic failure rat model. Animals were divided into five groups and pre-induced with phenobarbital (0.1 mg kg-1, i.p.) before administration of a single dose of acetaminophen (1 g kg-1, i.p.) except group 1 which was considered as normal. Group 2 was remained without treatment and considered as control while groups 3 to 5 were treated with SM (50 mg kg-1, p.o.), IMOD (30 mg kg-1, i.p.) and IMOD+SM, respectively 24 h post administration of acetaminophen. Blood was collected at 0, 24 and 72 h post acetaminophen treatment. Elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) confirmed hepatic failure induced by acetaminophen. After 48 h of treatment, the rats were anesthetized and the liver was removed and the right lobule was homogenized and then measured for catalase (CAT), malondialdehyde (MDA) and glutathione (GSH) value. Part of liver was left in paraffin for histopathology examination. CAT and GSH were significantly decreased in the acetaminophen-treated group while ALT, AST, ALP and MDA increased when compared to normals. Histopathological examination of acetaminophen-treated animals showed necrosis, inflammation, hyperplasia of kupffer and infiltration of mononuclear cells, dilation of sinusoids and disruption of hepatocytes, while treatment with IMOD+SM normalized protected hepatic architecture in accordance to biochemical results. Treatment of animals with IMOD and SM alone or in combinations considerably protected the hepatic failure by diminishing ALT, AST, ALP and MDA. Both IMOD and SM and their combination improved acetaminophen-induced histopathological hepatic damage. Conclusion is that combination of IMOD and SM considerably protect from acute hepatic failure via enzymatic and non-enzymatic mechanisms.
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