Gastrodin alleviates bone damage by modulating protein expression and tissue redox state

Area of Science:

• Biochemistry
• Toxicology
• Pharmacology

Background:

• Fluorosis is a prevalent disease impacting bone metabolism and enamel, with reactive oxygen species implicated in its pathogenesis.
• Gastrodin, known for its antioxidant properties, was investigated for its potential protective effects against fluoride-induced toxicity.

Purpose of the Study:

• To evaluate the efficacy of gastrodin in mitigating oxidative stress and bone tissue damage in a rat model of fluorosis.
• To determine the optimal dosage of gastrodin for therapeutic benefits in fluorosis.

Main Methods:

• Wistar rats were administered fluoride, followed by varying doses of gastrodin.
• Blood, bone, and teeth samples were collected at 2, 3, and 4 months post-treatment for analysis.
• Biochemical markers of oxidative stress (glutathione peroxidase, CAT, SOD) and apoptosis (caspase-3, caspase-9, Bax, Bcl-2) were assessed.

Main Results:

• Gastrodin treatment ameliorated oxidative stress and reduced fluoride accumulation in rats with fluorosis.
• A dosage of 400 mg·kg⁻¹ gastrodin significantly protected trabecular bone structure and reduced femur and alveolar bone injury.
• Gastrodin reversed fluoride-induced alterations in apoptotic markers, decreasing pro-apoptotic proteins (Bax, caspase-3, caspase-9) and increasing anti-apoptotic Bcl-2.

Conclusions:

• Gastrodin demonstrates significant protective effects against fluorosis-induced bone damage and oxidative stress in rats.
• The 400 mg·kg⁻¹ dosage of gastrodin is particularly effective in improving antioxidant capacity, reducing tissue fluoride levels, and modulating apoptosis.
• Gastrodin holds promise as a therapeutic agent for managing fluorosis.