الإجهاد التأكسدي في داء السكري ودور مضادات الأكسدة في الحد من مضاعفاته
DOI:
https://doi.org/10.54153/sjpas.2026.v8i1.1344الكلمات المفتاحية:
Oxidative stress، Antioxidant، diabetes mellitusالملخص
ينتج الإجهاد التأكسدي عن اختلال التوازن بين الجذور الحرة وأنظمة الدفاع المضادة للأكسدة المسؤولة عن معادلتها. وتُعد مضادات الأكسدة ضرورية لأنها تحدّ من تراكم الجذور الحرة، مما يسهم في تقليل الإجهاد التأكسدي داخل الجسم. ينشأ داء السكري من النوع الأول نتيجة عجز البنكرياس عن إنتاج الإنسولين بسبب التدمير المناعي الذاتي لخلايا بيتا (β) المفرزة للإنسولين. أما داء السكري من النوع الثاني فيتطور عبر مرحلتين رئيسيتين؛ إذ يبدأ بمقاومة الإنسولين في الأنسجة الطرفية، مما يحفّز زيادة إفراز الإنسولين كاستجابة تعويضية، تليها مرحلة تدهور تدريجي في وظيفة خلايا بيتا، يؤدي إلى عدم كفاية إنتاج الإنسولين واضطراب تنظيم سكر الدم. يتميّز كلا النوعين من داء السكري بفرط سكر الدم المزمن، والذي قد يؤدي في حال عدم السيطرة عليه إلى مضاعفات خطيرة. إن الارتفاع المستمر في مستويات الغلوكوز يعزّز توليد الجذور الحرة عبر عدة مسارات أيضية، من بينها تكوّن نواتج الغلَيكَة المتقدمة (AGEs)، وتنشيط مساري الهيكسوزأمين والبوليول، إضافة إلى الأكسدة الذاتية للغلوكوز. وتؤدي هذه المسارات مجتمعةً إلى زيادة شدة الإجهاد التأكسدي وتسهم في تطور المضاعفات الوعائية الدقيقة والكبيرة المرتبطة بداء السكري. وبناءً على ذلك، تؤدي مضادات الأكسدة دورًا داعمًا مهمًا من خلال اقتناص الجذور الحرة، وتقليل الضرر التأكسدي، وتعزيز القدرة المضادة للأكسدة في الجسم. ومع ذلك، لا تُعد مضادات الأكسدة علاجًا أساسيًا لداء السكري، وإنما تُستخدم كعوامل مساندة تساعد على الحد من الأذى الخلوي المرتبط بالإجهاد التأكسدي
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