Intravenous administration of recombinant Phα1ß: Antinociceptive properties and morphine tolerance reversal in a cancer-associated pain model.

Cancer-related pain is considered one of the most prevalent symptoms for those affected by cancer, significantly influencing quality of life and treatment outcomes. Morphine is currently employed for analgesic treatment in this case, however, chronic use of this opioid is limited by the development of analgesic tolerance and adverse effects, such as digestive and neurological disorders. Alternative therapies, such as ion channel blockade, are explored. The toxin Phα1ß has demonstrated efficacy in blocking calcium channels, making it a potential candidate for alleviating cancer-related pain. This study aims to assess the antinociceptive effects resulting from intravenous administration of the recombinant form of Phα1ß (r-Phα1ß) in an experimental model of cancer-related pain in mice, tolerant or not to morphine. The model of cancer-induced pain was used to evaluate these effects, with the injection of B16F10 cells, followed by the administration of the r-Phα1ß, and evaluation of the mechanical threshold by the von Frey test. Also, adverse effects were assessed using a score scale, the rotarod, and open field tests. Results indicate that the administration of r-Phα1ß provoked antinociception in animals with cancer-induced mechanical hyperalgesia, with or without morphine tolerance. Previous administration of r-Phα1ß was able to recover the analgesic activity of morphine in animals tolerant to this opioid. r-Phα1ß was proved safe for these parameters, as no adverse effects related to motor and behavioral activity were observed following intravenous administration. This study suggests that the concomitant use of morphine and r-Phα1ß could be a viable strategy for pain modulation in cancer patients.

Effects of gold nanoparticles administration through behavioral and oxidative parameters in animal model of Parkinson's disease.

Parkinson's disease (PD) is recognized as the second most common neurodegenerative disorder, after Alzheimer's disease. Reserpine administration to animals has been suggested as a PD model based on the effects of this monoamine-depleting agent on motor activity. Studies show that gold nanoparticles (GNPs) are effective for treating neurodegenerative diseases when used at certain concentrations. The objective of the present study was to evaluate the effects of GNPs administration under behavioral and oxidative stress conditions in an experimental model of PD. Fourty male C57BL/6 mice (20-30 g) were used, The animals were divided into four groups (N = 6): Sham; Sham and GNPs; Reserpine; Reserpine and GNPs. Three doses at the concentration of 0.25 mg/kg reserpine were administered subcutaneously at 48 h intervals. Treatment with GNPs was administered with 2.5 mg/kg GNPs (20 nm) for five consecutive days. Our results showed the therapeutic potential of GNPs, where the parameters observed in behavioral tests and oxidative stress were reverted in GNP-treated mice. It also partially improved neurotrophic factors, which are necessary for the survival of neurons. GNPs reversed the symptoms of PD caused by the use of alkaline reserpine in C57BL/6 mice, especially without toxicity. The results of this study suggest that GNPs could have clinical potential as an inhibitor of inflammation and oxidative stress in the CNS, thereby alleviating the secondary neurodegenerative processes and neuronal cell death caused by reserpine. These beneficial effects of GNPs provide support for new analyses to better understanding in the process of PD degeneration.