Buyang Huanwu Decoction
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Buyang Huanwu Decoction

Laurance Johnston, Ph.D.

Periodically, I’ve discussed various herbal or botanical approaches (i.e., phytomedicines) that promote neuronal health and regeneration. For example, one of mankind’s most commonly used herbal remedies Ginkgo biloba inhibits post-injury lipid peroxidation, a biochemical process that mediates further damage to the injured spinal cord. In another example, Mimosa pudica (sensitive or touch-me-not plant) is an herbal remedy of India’s ancient Ayurvedic healing tradition, which has been shown to stimulate peripheral-nerve regeneration.

In this update, I’ll discuss Buyang Huanwu Decoction (BYHWD), a Chinese herbal medicine that has been used for centuries to treat a variety of disorders, including paralysis. From a Traditional Chinese Medicine viewpoint, it’s used to invigorate the body, enhance blood circulation, and activate qi flow through energy meridians. The decoction contains extracts of various Chinese herbs, including astragalus (illustration), dong quai, red peony root, Rhizoma Chuanxiong, peach seed, safflower, and, perhaps the decoction’s crème de la crème, earthworm extract.

Demonstrating that ancient wisdom often has much validity, scientific studies indicate that BYHWD, indeed, exerts neuroprotective and regenerative effects. For example, animal research suggests that this herbal decoction can promote nerve regeneration after stroke and both peripheral-nerve and spinal-cord injuries.

In the case of SCI, Dr. An Chen et al (China) have evaluated BYHWD in a rat model of injury in which one side of the cord was transected at the cervical level (J Ethnopharmacol 2008; 117(3)). After transection, the rats were administered BYHWD or distilled water for eight weeks through a stomach tube. After this time period, the number of surviving neurons on the cord’s injured side for both BYHWD- and water-treated groups were compared to the neuron level on the non-injured side. Compared to the uninjured side, 78% of the neurons remained with the BYHWD-treated rats compared to only 58% of the water-treated rats. In other words, the BYHWD decoction reduced neuron loss from 42 to 22%.

In addition, cell bodies of surviving neurons atrophied by 64% in the water-treated controls compared with 35% in the BYHWD-treated rats. Hence, BYHWD enhanced the robustness of surviving neurons. 

Especially significantly, only in the BYHWD-treated rats did axons regenerate through the injury site. And, as expected with such regeneration, these rats recovered more forelimb function, the physical area affected by this experimental injury.

In another study, Dr. Lihong Fan and colleagues (China) evaluated the effects of BYHWD in a rabbit model of SCI (J Tradit Chin Med 2006; 26(2)). In this model, injury was generated by temporarily shutting off blood flow to the spinal cord’s lumbar region (i.e., ischemia), affecting hind-limb function. The rabbits were treated with either BYHWD or saline starting seven days before injury and continuing two days after injury. Hind-limb function was then measured using a scale ranging from 0 (complete paralysis) to 5 (normal function). Forty-eight hours after injury, the BYHWD-treated rabbits averaged 3.4 on this scale compared to 2.6 for the saline-treated controls.

With respect to peripheral-nerve injuries, Dr. Yueh-Sheng Chen et al (Taiwan) demonstrated that BYHWD stimulates growth in regenerating nerves (Am J Chin Med 2001; 29(3-4)). In this study, a 10-millimeter gap was created in the rat sciatic nerve (running down the leg from the back) and then bridged by a silicon-rubber tube. Regeneration across the gap was compared in BYHWD-treated rats and control animals who received no BYHWD. Nerves regenerated across the gap in 89% percent of the BYHWD-treated rats compared to only 70% of controls.

BYHWD may mediate its neuroprotective effects through several physiological mechanisms. For example, scientists have shown that BYHWD 1) stimulates the outgrowth and differentiation of neuronal stem-cell neurites (processes budding out from immature neurons, such as developing dendrites and axons); 2) inhibits apoptosis – a post-injury, programmed death of spinal-cord cells; and 3) decreases free radical generation and associated lipid peroxidation, biochemical processes that cause further damage to the injured cord.


Although these BYHWD-related improvements seem modest, it is important to note that studies have shown that substantial physical function can be retained even if only a relatively small proportion of neurons survive the injury. In this regard, we should also note that the post-injury putative standard of care methylprednisolone has statistically modest at best effectiveness - one senior scientist noting “Evidence of the drug's efficacy and impact is weak and may only represent random events” (Hurlbert RJ, J Neurosurg 93(1 suppl), 2000). Perhaps, given such reservations, we need to open-mindedly evaluate the therapeutic potential of various phytomedicines coming out of the wisdom of ancient healing traditions.

Adapted from article appearing in April 2009 Paraplegia News (For subscriptions, call 602-224-0500) or go to