Transdermal delivery of buprenorphine from reduced graphene oxide laden hydrogel to treat osteoarthritis.

The patients with chronic pain in osteoarthritis often have insufficient pain relief from non-opioids analgesics. Buprenorphine is a promising molecule for symptomatic relief of chronic pain. The marketed parenteral injections and sublingual tablets have short duration of action (half-life = 2.7 h), which is not suitable to manage chronic pain. The purpose of this research was to design buprenorphine-loaded Pluronic F127-reduced graphene oxide transdermal (noninvasive) hydrogel to achieve sustained release of buprenorphine to manage chronic pain in osteoarthritis. Pluronic F127 was used to stabilize the reduced graphene oxide in hydrogel system. The characterization studies including Fourier transform infrared spectroscopy, X-ray diffraction, and Raman spectroscopy confirmed the synthesis of Pluronic F127-reduced graphene oxide from graphite. The transmission electron microscopy image showed flat nanosheets of reduced graphene oxide (rGO). The developed hydrogel showed desirable pH, viscosity, adhesiveness, hardness, and cohesiveness for transdermal application. The ex vivo release study demonstrated the ability of the Pluronic F127-reduced graphene oxide (P-rGO) hydrogel to prolong release up to 14 days, owing to the strong π-π interactions between the graphene oxide (GO) and the buprenorphine. In cold ethanol tail flick model, the GO hydrogel showed sustained analgesic effect in comparison with hydrogel without rGO. Thus, this study demonstrated the potential of using Pluronic F127-reduced graphene oxide nanocarriers to prolong local analgesia for effective management for chronic pain.

Evaluation of antiarthritic activity of ginkgolic acid against Freund's adjuvant induced arthritic rat model

This study aimed to analyze the antiarthritic activity of ginkgolic acid against the Complete Freund's Adjuvant (CFA)-induced arthritis in rats. Arthritis was induced through an intradermal injection of CFA (0.1 mL) at the right hind footpad of adult Wistar Albino rats. Ginkgolic acid was administered orally at doses of 25 mg/kg and 50 mg/kg, respectively, once daily via gavage for 25 days upon inducing arthritis. Indomethacin was administered orally at a dose of 3 mg/kg twice in a week which served as positive control group. The animals were sacrificed and subjected to biochemical and histopathological analysis upon completion of treatment. Ginkgolic acid was able to reverse the arthritic effect (p < 0.01) induced by CFA in a dose dependent manner. Swelling of paw, thymus and spleen index, serum biomarker levels, and pro-inflammatory cytokines were significantly reduced (p < 0.01) by the acid whereas the antioxidant enzyme activities were remarkably restored. The histopathological findings were in agreement with the biochemical results. The results indicate that the antioxidant and anti-inflammatory properties of ginkgolic acid can be credited to the antiarthritic effects, and it can be promoted as a potential agent for therapeutic use against osteoarthritis