Azadeh Haghighitalab; Mahboubeh Kazemi Noughabi; Shima Minaee; Ahmad Amin; Ahmad Reza Bahrami
Abstract
Acute myocardial infarction (MI) describes as an irreversible death of heart muscle which is initiated by a shortage of myocardium oxygen supply and accompanies by a complex of pro- and anti-inflammatory events. During the last decades, innate and adaptive immune responses are considered ...
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Acute myocardial infarction (MI) describes as an irreversible death of heart muscle which is initiated by a shortage of myocardium oxygen supply and accompanies by a complex of pro- and anti-inflammatory events. During the last decades, innate and adaptive immune responses are considered more serious for controlling myocardial infarction. As, it was confirmed that deregulated immune system which triggers excessive local and systemic inflammatory events is responsible for serious adverse effects associated with acute MI. Bone marrow activation, spleen monocytopoiesis, a remarkable increase of circulating cytokines and adhesion molecules, in addition to elevated levels of active peripheral leukocytes and platelets are playing significant roles in determining the clinical outcome of patients with MI. The previous experience demonstrated the failure of traditional harsh anti-inflammatory strategies. High mortality rate and poor quality of life observed for survivors of MI despite current progress in the field highlight the urgent need for such interdisciplinary studies in the context of molecular cardiology. Hence, unraveling the cellular and molecular events which are involved in the management of inflammatory responses post-MI is of special focus. The concept of immune regulation after myocardial infarction is not new, but our perception for dealing with the challenge has been changed during the last decades with gaining more in-depth molecular/immunological knowledge. It seems that fine-tuning the interplay between innate and adaptive immune responses and regulating their cross-talk should be in special focus to establish effective therapeutic strategies.
Tahereh Sanjari; Toktam Hajjar; Madjid Momeni-Moghaddam
Abstract
Mesenchymal stem cells (MSCs) could differentiate into various types of tissues. These cells serve as a backup for the regeneration and repair of tissues or cells after injury. A skin wound is defined as an injury to the skin that needs to be restored. All types of cells in skin especially mesenchymal ...
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Mesenchymal stem cells (MSCs) could differentiate into various types of tissues. These cells serve as a backup for the regeneration and repair of tissues or cells after injury. A skin wound is defined as an injury to the skin that needs to be restored. All types of cells in skin especially mesenchymal stem cells play important role in wound healing process. In particular, paracrine signaling of MSC regulates the cellular responses at the wound site leading to reduction of inflammation, stimulation of angiogenesis and induction of cell migration and proliferation. Because of these abilities, MSCs are one of the most common stem cells for cell therapy in wound healing. This review focuses on the role of MSCs on wound healing process. In addition, major phases of wound repair and challenges of cell therapy are discussed.
Fatemeh Aghaei-Borashan; Mino Ilkhanipoor; Mohammad Hashemi; Farah Farrokhi1
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by joint swelling, synovial inflammation and joint destruction. Curcumin (diferuolymethane) is the most active component of Curcuma longa L. Several clinical trials have indicated curcumin to be a notable anti-inflammatory and ...
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Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by joint swelling, synovial inflammation and joint destruction. Curcumin (diferuolymethane) is the most active component of Curcuma longa L. Several clinical trials have indicated curcumin to be a notable anti-inflammatory and antioxidant compound. Therefore the aim of this study is investigating the effects of curcumin on levels of inflammation and inflammatory biomarkers in arthritic rats.
Arthritis was induced by subcutaneous injection of Freund’s complete adjuvant (0.5 mL) into the right hind paw of Wistar male rats. Animals were divided into four groups (n=8). GroupI acted as control, group II arthritic rats received vehicle, group III arthritic rats were treated with curcumin (30 mg/kg, orally) and another group arthritic rats were treated with indomethacin (3 mg/kg, orally) seven days after injection of Freund’s Complete Adjuvant for 15 days. The changes caused by chronic inflammation were evaluated by measurement of the ankle circumference three times per week. At the end of the experimental period, blood samples were collected by cardiac puncture to determine erythrocyte sedimentation rate, C.reactive protein levels and White blood cells count.
An increase in erythrocyte sedimentation rate, C. reactive protein concentrations, White blood cells count and ankle circumference was observed in arthritic rats compared with control rats (p
