مدولاسيون بيان ژن تومور نكروز فاكتور آلفاناشي از پرتو در نخاع گردني موش توسط ملاتونين

عنوان انگليسی

Modulation of Radiation – Induced tumor necrosis factor α (TNF-α) Gene Expression in the Rats Spinal Cord by Melatonin

خلاصه انگلیسی

The spinal cord is the major dose- limiting organ for radiotherapy of cancer in the head and neck region. Understanding the cellular and molecular mechanisms may help to develop strategies to either increase the radiation tolerance or to treat spinal cord alterations induced by irradiation. Radiation exposure leads to oxidative stress and necrosis in many cell types including neurons. Radiation – induced apoptosis has also been observed in animal models. The exact mechanism and the genes that are activated in the process of radiation- induced apoptosis has not established yet. However many events that occur at the cell surface and intracellular during apoptosis in the nervous system have been reported. There is literature to support possible roles for TNF- α contributor to apoptosis in the CNS. In the last decade, there have been reports on the anti apoptotic effect of melatonin, an endogenous compound mainly synthesized by the pineal gland in the human brain. The purpose of this study was to investigate changes in TNF-α in the spinal cord after neck irradiation with 22 Gy. In addition, we evaluated the ability of melatonin to modulate the radiation - induced TNF-α gene expression in this animal model of spinal cord irradiation. A number of rats were divided into four groups: 1. Control group; 2. Group that was treated with intraperitonial injection of melatonin; 3.Group of rats which got melatonin 30 min. prior to cervical spinal cord gamma irradiation at a dose of 22 Gy; and 4.Group that was given an intraperitonial injection of vehicle and the spinal cord radiation. The expression of TNF- α was evaluated by real time reverse transcription polymerase chain reaction (Real time RT-PCR). The finding indicates that melatonin down-regulates the TNF- α gene expression in the spinal cord in response to radiation.

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