شنبه 1 دی 1403
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دوره 32، شماره 151 - ( 12-1402 )
جلد 32 شماره 151 صفحات 162-154 |
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Ghashghaie M S, Ebrahimi M, Eidi M. Royal Jelly Enhances Skin Wound Healing in Mice Model by Modulating Glutathione Peroxidase Activity and CCL2 Chemokine Gene Transcription. J Adv Med Biomed Res 2024; 32 (151) :154-162
URL: http://journal.zums.ac.ir/article-1-7228-fa.html
URL: http://journal.zums.ac.ir/article-1-7228-fa.html
Royal Jelly Enhances Skin Wound Healing in Mice Model by Modulating Glutathione Peroxidase Activity and CCL2 Chemokine Gene Transcription. Journal of Advances in Medical and Biomedical Research. 1402; 32 (151) :154-162
چکیده: (317 مشاهده)
Background & Objective: Wound healing can be impaired by diabetes and aging, leading to delays, scarring, or infections. There is a need for improved treatments to expedite wound healing. Complementary and alternative medicine often utilizes natural remedies for disease management. Royal jelly (RJ), a natural bee product, is a food supplement known for its beneficial biomedical properties. CCL2 exhibits angiogenic properties and has been observed to promote tissue regeneration. Glutathione peroxidase (GPx) plays a critical role in tissue repair by preventing apoptosis and tissue damage caused by excessive reactive oxygen species (ROS) production. This study investigates the application of Royal Jelly to accelerate skin wound healing through modulation of GPx activity and CCL2 expression.
Materials & Methods: Thirty mice were divided into six groups. Royal jelly treatment (2.5, 10, and 40 mg/kg) was administered orally. Following the treatment period, GPx activity was measured in blood samples, and the transcription level of the CCL2 gene was assessed in healing wound tissue samples using real-time PCR. Evaluation of epithelial tissue formation and the presence of inflammatory and fibroblastic cells was conducted in prepared wound tissue sections.
Results: Analysis of wound diameter revealed that oral administration of RJ (10 and 40 mg/kg) significantly accelerated wound healing (P=0.0198). Moreover, GPx activity in the royal jelly groups (2.5, 10, and 40 mg/kg) was significantly lower (43.8, 68.6, and 31.1, respectively) compared to the PC group (P=0.0001). Additionally, CCL2 mRNA levels in the royal jelly groups (2.5, 10, and 40 mg/kg) were significantly higher (1.9, 6.6, and 15.2 times, respectively) than in the PC group (P<0.05). Administration of 40 mg/kg of royal jelly significantly increased fibroblast cells in tissue sections.
Conclusion: Royal jelly, as a complementary food drug, facilitates wound healing by promoting the proliferation and migration of fibroblasts, regulating ROS production, and stimulating CCL2 gene transcription.
Materials & Methods: Thirty mice were divided into six groups. Royal jelly treatment (2.5, 10, and 40 mg/kg) was administered orally. Following the treatment period, GPx activity was measured in blood samples, and the transcription level of the CCL2 gene was assessed in healing wound tissue samples using real-time PCR. Evaluation of epithelial tissue formation and the presence of inflammatory and fibroblastic cells was conducted in prepared wound tissue sections.
Results: Analysis of wound diameter revealed that oral administration of RJ (10 and 40 mg/kg) significantly accelerated wound healing (P=0.0198). Moreover, GPx activity in the royal jelly groups (2.5, 10, and 40 mg/kg) was significantly lower (43.8, 68.6, and 31.1, respectively) compared to the PC group (P=0.0001). Additionally, CCL2 mRNA levels in the royal jelly groups (2.5, 10, and 40 mg/kg) were significantly higher (1.9, 6.6, and 15.2 times, respectively) than in the PC group (P<0.05). Administration of 40 mg/kg of royal jelly significantly increased fibroblast cells in tissue sections.
Conclusion: Royal jelly, as a complementary food drug, facilitates wound healing by promoting the proliferation and migration of fibroblasts, regulating ROS production, and stimulating CCL2 gene transcription.
نوع مطالعه: مقاله پژوهشی |
موضوع مقاله:
Life science
دریافت: 1402/1/26 | پذیرش: 1402/11/7 | انتشار: 1402/12/12
دریافت: 1402/1/26 | پذیرش: 1402/11/7 | انتشار: 1402/12/12
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