اثرات حفاظتی پنتوکسی‌فیلین بر مرگ سلولی القا شده توسط مت‌آمفتامین در سلول‌های PC12

نویسندگان

  • کمیل امینی - گروه بیوتکنولوژی، دانشکده علوم و فناوری‌های زیستی، دانشگاه اصفهان، اصفهان، ایران. orcid https://orcid.org/0000-0001-7500-8187
  • حسین ژاله - مرکز تحقیقات پیشگیری سوءمصرف مواد، دانشگاه علوم پزشکی کرمانشاه، کرمانشاه، ایران. orcid https://orcid.org/0000-0003-0974-8480
  • محمدرضا نورایی - مرکز تحقیقاتی نانوبیوتکنولوژی، دانشگاه علوم پزشکی بقیه‌الله، تهران، ایران. orcid https://orcid.org/0000-0003-1394-6412
  • رمضانعلی طاهری - مرکز تحقیقاتی نانوبیوتکنولوژی، دانشگاه علوم پزشکی بقیه‌الله، تهران، ایران. orcid https://orcid.org/0000-0003-1394-6412

DOI::

https://doi.org/10.22100/jkh.v18i1.3076

کلمات کلیدی:

مت آمفتامین, پنتوکسی فیلین, آپوپتوزیس, مرگ سلولی

چکیده

مقدمه: سوء مصرف مت‌آمفتامین یک نگرانی جهانی در چند دهه اخیر بوده است. 5/3 میلیون نفر تحت تأثیر سوء مصرف مت‌آمفتامین قرار گرفته‌اند و این مسأله در حال افزایش است. مت‌آمفتامین موجب القای آپوپتوز در اکثر رده‌های سلولی می‌شود. به‌نظر می‌رسد پنتوکسی‌فیلین به‌عنوان یک مهارکننده فسفودی استراز، توانایی کاهش التهاب را در نتیجه توانایی کاهش مرگ سلولی ناشی از مت‌آمفتامین در سلول‌های عصبی را دارد.

مواد و روش ها: در این مطالعه، سلول‌های PC12 در محیط کشت DMEM رشد داده شدند. از آزمون MTT برای بقای سلول، آزمون LDH برای اندازه‌گیری سمیت سلولی، کیت سنجش رنگ‌سنجی فعالیت کاسپاز (Bio-techne) برای تشخیص فعالیت کاسپاز 3، رودامین 123 برای تشخیص پتانسیل غشای میتوکندری و میکروسکوپ فلورسانس برای اندازه‌گیری فعالیت آنزیم‌های آنتی‌اکسیدانی استفاده کردیم.

نتایج: پنتوکسی‌فیلین باعث افزایش بقای سلولی و جذب رودامین-123 و کاهش سمیت سلولی و فعالیت کاسپاز-3 در تمام غلظت‌های 1 نانومولار تا 100 میکرومولار شد و غلظت بهینه آن 100 میکرومولار می‌باشد (05/0<P).

نتیجهگیری: پنتوکسی‌فیلین به‌عنوان یک مهارکننده فسفودی استراز می‌تواند با اثرات ضدالتهابی خود، مرگ سلولی ناشی از مت‌آمفتامین را به میزان قابل‌توجهی کاهش دهد.

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