Objective: This study aims to experimentally evaluate the impact of 20(S)-ginsenoside Rg3 on the progression of neuropathy induced by streptozotocin (STZ)-induced diabetes.
Materials and Methods: Adult male Wistar rats were randomly divided into three groups: con-trol, untreated diabetic, and 20(S)-ginsenoside Rg3-treated diabetic groups (n=6 each). The rats were intraperitoneally injected with a single dose of STZ (50 mg/kg) to induce diabetes, which was verified by the presence of hyperglycemia (>300 mg/dl). Treatment involved administering a daily dose of 20(S)-ginsenoside Rg3 at 5 mg/kg/day through oral gavage for five weeks. Control rats received an equivalent volume of saline phosphate buffer (pH 7.4). Nociceptive alterations were assessed using tail flick and hot plate tests in the fourth week. Distal latency and nerve con-duction velocity were measured in vivo from the exposed sciatic nerve in the fifth week.
Results: While STZ-induced diabetes led to a significant decline in body weight, an increase in blood glucose levels, and delays in both sensory and motor responses, 20(S)-ginsenoside Rg3 treatment favorably corrected these adverse effects. This treatment effectively alleviated weight loss, lowered blood glucose levels, protected the sciatic nerve, and thus clearly demonstrated a protective role against the progression of neuropathy.
Conclusion: Treatment with 20(S)-ginsenoside Rg3 holds the potential to be used as a neuro-protective agent for diabetic neuropathy. It may also exert preventive actions against post-dia-betic events at the molecular level, and the mechanisms underlying these actions need further exploration.