ArticleActa pharmacologica Sinica2011
Involvement of cholinergic system in suppression of formalin-induced inflammatory pain by cobratoxin.
Article in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Exploring the Pain-Relieving Potential: Unveiling Antinociceptive Properties in Animal Venoms and Toxins.Toxins · 2026Review
- Snake Venom: A Promising Source of Neurotoxins Targeting Voltage-Gated Potassium Channels.Toxins · 2023Review
- Current Drug Development Overview: Targeting Voltage-Gated Calcium Channels for the Treatment of Pain.International journal of molecular sciences · 2023Review
- Phenolic Composition, Wound Healing, Antinociceptive, and Anticancer Effects ofMolecules (Basel, Switzerland) · 2023Article
- Nicotinic acetylcholine signaling is required for motor learning but not for rehabilitation from spinal cord injury.Neural regeneration research · 2023Article
- Neurotoxins Acting at Synaptic Sites: A Brief Review on Mechanisms and Clinical Applications.Toxins · 2022Review
- NFAT5 Deficiency Alleviates Formalin-Induced Inflammatory Pain Through mTOR.International journal of molecular sciences · 2021Article
- The Spinal α7-Nicotinic Acetylcholine Receptor Contributes to the Maintenance of Cancer-Induced Bone Pain.Journal of pain research · 2021Article
- Review
- The Effects of Isolated Fractions ofJournal of arthropod-borne diseases · 2017Article
- Cobrotoxin from Naja naja atra Venom Ameliorates Adriamycin Nephropathy in Rats.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Suppression of Inflammation and Arthritis by Orally Administrated Cardiotoxin from Naja naja atra.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Differential Effects of Naja naja atra Venom on Immune Activity.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- The Protective Effects of Cobra Venom from Naja naja atra on Acute and Chronic Nephropathy.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Antinociceptive and anti-inflammatory effects of orally administrated denatured naja naja atra venom on murine rheumatoid arthritis models.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Article
- Reduced Pain Responses With a Digital Automatic Syringe: Behavioral and Molecular Evidence in a Rodent Formalin Model.In vivo (Athens, Greece)Article
- Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the analgesic effect of cobratoxin (CTX), a long-chain α-neurotoxin from Thailand cobra venom, in a rat model of formalin-induced inflammatory pain.
methodsInflammatory pain was induced in SD rats via injecting 5% formalin (50 μL) into the plantar surface of their right hind paw. CTX and other agents were ip administered before formalin injection. The time that the animals spent for licking the injected paw was counted every 5 min for 1 h.
resultsCTX (25, 34, and 45 μg/kg) exhibited a dose-dependent analgesic effect during the phase 1 (0-15 min) and phase 2 (20-60 min) response induced by formalin. Pretreatment with naloxone (0.5 or 2.5 mg/kg) did not block the analgesic effect of CTX. Pretreatment with atropine at 5 mg/kg, but not at 2.5 mg/kg, antagonized the analgesic effect of CTX. Treatment with the nonselective nAChR antagonist mecamylamine (3 mg/kg) inhibited the analgesic effects of CTX in Phase 1 and Phase 2 responses, while with the selective α7-nAChR antagonist methyllycaconitine (3 mg/kg) antagonized the effect of CTX only in the Phase 1 response. Treatment with the α7-nAChR agonist PNU282987 (3 mg/kg) significantly reduced the formalin-induced phase 2 pain response, but only slightly reduced the Phase 1 pain response.
conclusionThe results suggest that CTX exerts an antinociceptive effect in formalin-induced inflammatory pain, which appears to be mediated by mAChR and α7-nAChR.
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