Effects of Ginger on Advanced Glycation End-Products and Inflammation in the Ovarian Tissue of Streptozotocin-Induced Diabetic Rats

Advanced glycation end products (AGEs) and inflammation play a crucial role in the progression of diabetic complications, including ovarian disorders. The current research investigated the potential impact of hydroalcoholic extract of ginger (Zingiber Officinale) on hyperglycemia-induced AGEs and inflammatory markers.

A total of 96 female Wistar rats were randomized into four groups (n=24 in each group) as follows: 1) control, 2) diabetes, 3) diabetes + 200 mg/kg ginger, 4) diabetes + 400 mg/kg ginger. Streptozotocin (STZ) - induced diabetic rats, as our experimental model for diabetes, orally received 200 or 400 mg/kg/day ginger extract for eight weeks. At the end of the treatment period, body weight, ovarian weight, serum AGEs level, ovarian RAGE, IL-1β, and TNF-α mRNA levels were measured.

At the end of the study, diabetic rats exhibited an obvious decrease in body weight (P < 0.01) and ovarian weight (P < 0.01) compared to normal rats. However, ginger supplementation (200 mg/kg) exhibited a significant increment in ovarian weight (P < 0.05) and body weight (P < 0.01). These changes were also more pronounced in the diabetic rats treated with 400 mg/kg ginger extract (P < 0.01). Serum AGEs (P < 0.001) and ovarian RAGE (P < 0.01), IL-1β (P < 0.01), and TNF-α (P < 0.01) mRNA levels were significantly elevated in diabetic rats compared with control group. Administration of the diabetic group with 200 mg/kg ginger extract significantly ameliorated the serum level of AGEs (P < 0.01) and the transcript levels of RAGE (P < 0.05), TNF-α (P < 0.01) and IL-1β (P < 0.05). The 400 mg/kg ginger extract dose remarkably alleviated AGEs (P < 0.001) in the serum and RAGE (P < 0.01), TNF-α (P < 0.01), and IL-1β (P < 0.01) in the ovary of diabetic rats.

The present study's findings revealed that daily administration of ginger extract reduces AGEs and the transcript levels of RAGE and inflammatory markers in the STZ- induced female rats.