aconitine and Neoplasms

To explore the effect of lappaconitine on patient-controlled intravenous analgesia (PCIA) and serum complement 3 and 4 (C3 and C4) levels of cancer patients undergoing rectum surgery.. Totally 60 patients, who were scheduled for rectum carcinoma surgery, were recruited to the study and assigned in 3 groups, the blank control group, the tramadol group, and the lappaconitine group, 20 in each group. Lappaconitine (8 mg) was intravenously dripped to patients in the lappaconitine group 30 min before ending the operation. PCIA started as soon as the end of the surgery and the total dose of lappaconitine was 36 mg. Patients of the tramadol group were treated with tramadol (100 mg) intravenously within 30 min before ending the operation. The dripping was completed within 30 min. PCIA was started as soon as the end of the surgery and the total dose of lappaconitine was 36 mg. Tramadol (100 mg) was intravenously dripped to patients in the tramadol group 30 min before ending the operation. PICA was started as soon as the end of the surgery and the total dose of tramadol was 900 mg. Pethidine (50 mg) and droperidol (2. 5 mg) was intramuscularly injected to patients in the blank control group for pain relief according to their complaints. Pain degrees were assessed by visual analog scale (VAS) 12 h before surgery, 12, 24, 48, and 72 h after surgery. Blood samples were withdrawn at the same time point. Contents of serum C3 and C4 were determined by immunoturbidimetry.. VAS scores of the blank control group were significantly higher after surgery than before surgery (P <0. 01). There was no statistical difference in VAS scores between before surgery and after surgery in the tramadol group and the lappaconitine group (P >0. 05). VAS scores were significantly lower at each post-surgery time point in the tramadol group and the lappaconitine group than in the blank control group with statistical difference (P < 0.01). There was no statistical difference in VAS scores at each post-surgery time point between the tramadol group and the lappaconitine group (P >0. 05). Compared with before surgery, contents of serum C3 and C4 significantly decreased in all of the three groups at 12, 24, and 48 h after surgery (P < 0.05, P < 0.01). They recovered to the pre-surgery level till 72 h after surgery (P > 0.05). Serum C3 and C4 contents at 48 h after surgery were higher in the tramadol group than in the blank control group (P < 0.05). Serum C3 and C4 contents at 24 and 48 h after surgery were higher in the lappaconitine group than in the blank control group (P < 0.05). There was no statistical difference in serum C3 and C4 contents at each time point between the tramadol group and the lappaconitine group (P > 0.05). VAS scores were obviously negatively correlated with serum contents of C3 and C4 (r = -0.622, r = -0.649, P < 0.01).. Lappaconitine (used at the dose in this study) showed better pain relief effect after surgery. Besides, it could inhibit the surgic wound and pain, and elevate serum contents of C3 and C4.

Topics: Aconitine; Analgesia, Patient-Controlled; Analgesics, Non-Narcotic; Complement C3; Digestive System Surgical Procedures; Humans; Neoplasms; Orthopedic Procedures; Pain Measurement; Pain, Postoperative; Postoperative Period; Rectum; Tramadol

Patients suffering from cancer induced bone pain (CIBP) have a poor quality of life that is exacerbated by the lack of effective therapeutic drugs. Monkshood is a flowering plant that has been used in traditional Chinese medicine where it has been used to relieve cold pain. Aconitine is the active component of monkshood, but the molecular mechanism for how this compound reduces pain is unclear.. In this study, we employed molecular and behavioral experiments to explore the analgesic effect of aconitine. We observed aconitine alleviated cold hyperalgesia and AITC (allyl-isothiocyanate, TRPA1 agonist) induced pain. Interestingly, we found aconitine directly inhibits TRPA1 activity in calcium imaging studies. More importantly, we found aconitine alleviated cold and mechanical allodynia in CIBP mice. Both the activity and expression of TRPA1 in L4 and L5 DRG (Dorsal Root Ganglion) neurons were reduced with the treatment of aconitine in the CIBP model. Moreover, we observed aconiti radix (AR) and aconiti kusnezoffii radix (AKR), both components of monkshood that contain aconitine, alleviated cold hyperalgesia and AITC induced pain. Furthermore, both AR and AKR alleviated CIBP induced cold allodynia and mechanical allodynia.. Taken together, aconitine alleviates both cold and mechanical allodynia in cancer induced bone pain via the regulation of TRPA1. This research on the analgesic effect of aconitine in cancer induced bone pain highlights a component of a traditional Chinese medicine may have clinical applications for pain.

Topics: Aconitine; Analgesics; Animals; Cancer Pain; Hyperalgesia; Mice; Neoplasms; Pain; Quality of Life; TRPA1 Cation Channel

The nicotinic acetylcholine receptor (nAChR) was first characterized in 1970 as a membrane receptor of a neurotransmitter and an ion channel. nAChRs have been shown to be involved in smoking-induced cancer formation in multiple types of human cancer cells. In vitro and in vivo animal studies have shown that homopentameric nAChR inhibitors, such as methyllycaconitine and α-Bgtx, can attenuate nicotine-induced proliferative, angiogenic, and metastatic effects in lung, colon, and bladder cancer cells. Recent publications have shown that α9-nAChR is important for breast cancer formation, and in many in vivo studies, α9-nAChR-specific antagonists (e.g., α-ImI, α-ImI, Vc1.1, RgIA, and It14a) produced an analgesic effect. Vc1.1 functions in a variety of animal pain models and currently has entered phase II clinical trials. For cancer therapy, natural compounds such as garcinol and EGCG have been found to block nicotine- and estrogen-induced breast cancer cell proliferation through inhibition of the α9-nAChR signaling pathway. A detailed investigation of the carcinogenic effects of nAChRs and their specific antagonists would enhance our understanding of their value as targets for clinical translation.

Topics: Aconitine; Anticarcinogenic Agents; Catechin; Humans; Molecular Targeted Therapy; Neoplasms; Nicotinic Antagonists; Receptors, Nicotinic; Signal Transduction; Smoking; Terpenes