The formalin-induced pain model is a commonly used pain model. It involves injecting an appropriate amount of formalin into the subcutaneous tissue of the dorsal hind paw of a mouse, and pain-related behavior is assessed by measuring the time the mouse spends licking the injected paw. Formalin-induced nociceptive behavior consists of two distinct phases (Phase I occurs approximately 10 minutes post-injection, while Phase II begins around 15–20 minutes after injection and lasts for over 60 minutes). Non-steroidal anti-inflammatory drugs (NSAIDs) are ineffective against Phase I pain but can attenuate Phase II pain. This type of pain is generally considered to be associated with central sensitization. Studying such pain is critically important for understanding the mechanisms of hyperalgesia resulting from tissue injury in clinical settings.
Fig1. Formain induced pain models. Pain-like behaviors were observed in mice within minutes of injection, manifested by licking the soles of the feet. The formalin pain model is acute and the pain goes away within hours.
Carrageenan (also known as lambda carrageenan, CG) is a potent chemical agent used to stimulate the release of inflammatory and pro-inflammatory mediators, including prostaglandins, leukotrienes, histamine, serotonin, bradykinin, and TNF-α, among others. Injection of carrageenan into the paw, muscle, joint, or other sites of experimental animals initially induces acute inflammation, which can transition into chronic inflammation after two weeks. This model is primarily used to study acute inflammatory pain and to simulate conditions of tissue injury, such as joint sprain, strain, and myositis.
Fig1. Carrageenan-induced pain models. Mice exhibit mechanical algesia and thermal algesia after injection. The chronic inflammatory pain model induced by carrageenan can last for days.
The Spared Nerve Injury (SNI) model is established by ligating a subset of the sciatic nerve branches. This model robustly and persistently recapitulates alterations in mechanical and thermal sensitivity. Furthermore, the SNI model faithfully reproduces many of the clinical features associated with neuropeptides.
Fig1. SNI surgery induced neuropathic pain model. The SNI mouse model involves ligation of two of the three branches of the sciatic nerve (the tibial nerve and the common peroneal nerve), while the sural nerve is left intact . The lesion results in marked hypersensitivity in the lateral area of the paw, which is innervated by the spared sural nerve. Painful symptoms can last for months.
Bone pain is one of the most common types of pain experienced by cancer patients. The mechanisms underlying pain in patients with bone metastases are complex, involving various interactions among tumor cells, bone cells, activated inflammatory cells, and neurons innervating the bone. The mouse model of bone cancer pain induced by tibial injection is currently considered an ideal animal model for studying bone cancer pain, owing to its phenotypic similarity to clinical symptoms in patients and the simplicity of pain assessment methods. SMOC offers a variety of bone cancer pain models induced by different tumor cell lines, including osteosarcoma cells and breast cancer cells.
Fig1. Idiopathic pain model induced by bone metastatic cancer. 231 cells were injected into the bone marrow cavity of the femur, and spontaneous pain and algesia could be observed in some of the mice 14 days after injection, and in almost all of the mice 21 days after injection. After treated some of the mice exhibiting pain with gabapentin for one week, there was a significant relief of spontaneous pain behaviour and algesia/hypersensitivity in the administered group of mice.
