Abstract
Amyotrophic lateral sclerosis (ALS) is caused by the degeneration of lower and upper motor neurons, leading to muscle paralysis and respiratory failure. However, there is no effective drug or therapy to treat ALS. Complementary and alternative medicine (CAM), including acupuncture, pharmacopuncture, herbal medicine, and massage is popular due to the significant limitations of conventional therapy. Bee venom acupuncture (BVA), also known as one of pharmacopunctures, has been used in Oriental medicine to treat inflammatory diseases. The purpose of this study is to investigate the effect of BVA on the central nervous system (CNS) and muscle in symptomatic hSOD1G93A transgenic mice, an animal model of ALS. Our findings show that BVA at ST36 enhanced motor function and decreased motor neuron death in the spinal cord compared to that observed in hSOD1G93A transgenic mice injected intraperitoneally (i.p.) with BV. Furthermore, BV treatment at ST36 eliminated signaling downstream of inflammatory proteins such as TLR4 in the spinal cords of symptomatic hSOD1G93A transgenic mice. However, i.p. treatment with BV reduced the levels of TNF-α and Bcl-2 expression in the muscle hSOD1G93A transgenic mice. Taken together, our findings suggest that BV pharmacopuncture into certain acupoints may act as a chemical stimulant to activate those acupoints and subsequently engage the endogenous immune modulatory system in the CNS in an animal model of ALS.
Highlights
Amyotrophic lateral sclerosis (ALS) is caused by the selective and progressive loss of motor neurons, leading to irreversible paralysis; speech, swallowing and respiratory malfunction; and eventually the death of the affected individual after a rapid disease course
Our findings suggest that Bee venom (BV) pharmacopuncture into certain acupoints may act as a chemical stimulant that activates the acupoint and subsequently engages the endogenous immune modulatory system in the central nervous system (CNS) of an ALS animal model
The mice were divided into four groups: non-transgenic mice treated with saline at ST36, Non-Tg, n = 9; hSOD1G93A mice treated with saline at ST36, CON, n = 10; hSOD1G93A mice treated with Bee venom acupuncture (BVA) at ST36, ST36, n = 10; and hSOD1G93A mice injected i.p. with BV, i.p. administration of BV (IP), n = 10
Summary
Amyotrophic lateral sclerosis (ALS) is caused by the selective and progressive loss of motor neurons, leading to irreversible paralysis; speech, swallowing and respiratory malfunction; and eventually the death of the affected individual after a rapid disease course. (SOD1) cause 15%–20% of familial ALS (fALS) cases, corresponding to 1%–2% of all ALS cases [1]. Several studies related to neuroinflammation by microglia and astrocytes have reported that inflammation is fundamental to the pathogenesis of ALS and have suggested that anti-inflammatory drugs may play an important role in treating ALS patients [7,8,9]. Anti-inflammatory agents including celastrol, thalidomide, lenalidomide, NDGA, and pioglitazone have delayed the progress of disease in ALS animal models but require further evaluation in clinical studies [10]
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