Medical Research
Bee Venom at St36 reduces autoimmune encephalomyelitis
Kristen Sparrow • January 17, 2015
Bee venom has been used traditionally in Chinese Medicine for decades but it seems to be getting more “buzz” lately. (pardon the pun) This article shows that the bee venom needs to be injected into Stomach 36 for it to work, not in other acupuncture points. Stomach 36 is the classic point (earth of the earth for post celestial constitution) for immunity. I would have predicted some effect from any acupuncture point, so I may need to reconsider my mental models.
Mol Neurobiol. 2015 Jan 13. [Epub ahead of print]
Bee Venom Acupuncture Alleviates Experimental Autoimmune Encephalomyelitis by Upregulating
Regulatory T Cells and Suppressing Th1 and Th17 Responses.
Author information
- 1Department of Cancer Preventive Material Development, College of Oriental Medicine, Kyung Hee University, Seoul, 130-701, Republic of Korea.
Abstract
The protective and therapeutic mechanism of bee venom acupuncture (BVA) in neurodegenerative disorders is not clear. We investigated whether treatment with BVA (0.25 and 0.8 mg/kg) at the Zusanli (ST36) acupoints, located lateral from the anterior border of the tibia, has a beneficial effect in a myelin basic protein (MBP)68-82-induced acute experimental autoimmune encephalomyelitis (EAE) rat model. Pretreatment (every 3 days from 1 h before immunization) with BVA was more effective than posttreatment (daily after immunization) with BVA with respect to clinical signs (neurological impairment and loss of body weight) of acute EAE rats. Treatment with BVA at the ST36 acupoint in normal rats did not induce the clinical signs. Pretreatment with BVA suppressed demyelination, glial activation, expression of cytokines [interferon (IFN)-γ, IL-17, IL-17A, tumor necrosis factor-alpha (TNF-α), and IL-1β], chemokines [RANTES, monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein (MIP)-1α], and inducible nitric oxide synthase (iNOS), and activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB (p65 and phospho-IκBα) signaling pathways in the spinal cord of acute EAE rats. Pretreatment with BVA decreased the number of CD4+, CD4+/IFN-γ+, and CD4+/IL-17+ T cells, but increased the number of CD4+/Foxp3+ T cells in the spinal cord and lymph nodes of acute EAE rats. Treatment with BVA at six placebo acupoints (SP9, GB39, and four non-acupoints) did not have a positive effect in acute EAE rats. Interestingly, onset and posttreatment with BVA at the ST36 acupoint markedly attenuated neurological impairment in myelin oligodendrocyte glycoprotein (MOG)35-55-induced chronic EAE mice compared to treatment with BVA at six placebo acupoints. Our findings strongly suggest that treatment with BVA with ST36 acupoint could delay or attenuate the development and progression of EAE by upregulating regulatory T cells and suppressing T-helper (Th) 17 and Th1 responses. These results warrant further investigation of BVA as a treatment for autoimmune disorders of the central nervous system.
