Sulfur dioxide reduces hippocampal cells death and improves learning and memory deficits in rat model of transient global ischemia/reperfusion

  • سال انتشار: 1397
  • محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 21، شماره: 10
  • کد COI اختصاصی: JR_IJBMS-21-10_003
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 170
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نویسندگان

Fatemeh Zare Mehrjerdie

Neurobiomedical Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran

Ali Shoshtari

Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran

Fahimeh Mohseni

School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran

Hossein Khastar

School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran

Pirasteh Norouzi

School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran

Yasin Asadi

Laboratory of Learning and Memory, Physiology Research Center and Physiology Department, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran

Masoumeh Dadkhah

Laboratory of Learning and Memory, Physiology Research Center and Physiology Department, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran

Mehdi Khaksari

Addiction Research Center, Shahroud University of Medical Sciences, Shahroud, Iran

چکیده

Objective(s): According to recent the findings, sulfur dioxide (SO۲) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO۲ exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO۲ following global cerebral ischemia/reperfusion (I/R).Materials and Methods: Forty-eight male Wistar rats that weighed ۲۶۰–۳۰۰ g, were randomly allocated into ۴ groups: sham group (n=۱۲), I/R group (n=۱۲), and I/R+SO۲ groups (NaHSO۳ and Na۲SO۳; ۱:۳ ratio; ۵ and ۱۰ µg/kg, respectively; for ۳ days, n=۱۲). Cerebral ischemia model was prepared by occlusion of both common carotid arteries for ۲۰ min. Saline as a vehicle and SO۲ donor at doses ۵ µg/kg (intraperitoneally) were injected for ۳ days after reperfusion. Four days after ischemia, the passive avoidance memory test was carried out in four groups, and after behavioral assessment, necrosis, apoptosis, and antioxidant enzyme analysis were carried out.Results: SO۲ treatment could significantly improve memory impairments in rats with cerebral ischemia/reperfusion (I/R) (P< ۰.۰۵). An increase in both superoxide dismutase and glutathione and a reduction in malondialdehyde were reported in the SO۲ group versus the ischemic group (P< ۰.۰۵). Moreover, SO۲ could significantly decrease necrotic and apoptotic cells in the CA۱ region (P< ۰.۰۱). Conclusion: According to the findings, SO۲ exerts significant neuroprotective effects on cerebral I/R due to its antioxidant activity.

کلیدواژه ها

Antioxidant activity, Apoptosis, Brain ischemia, Memory, Sulfur dioxide

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