The new research in mice suggests that supplementation with either green tea polyphenols or alfacalcidol (1-alpha-OH-vitamin D3) may reverse damage to bones caused by lipopolysaccharide induced chronic inflammation, while combining the ingredients may sustain bone micro-architecture and strength, according to new findings published in The Journal of Nutritional Biochemistry.
According to the authors, led by Dr Chwan-Li Shen from Texas Tech University Health Sciences Center, the study also shows that the improvement in bone micro-architecture and quality along with the down-regulation bone TNF-alpha expression mechanism further corroborate the anti-inflammatory role of green tea polyphenols and 1-alpha-OH-vitamin D3 (alfacalcidol) in skeletal health – which may reduce the risk of osteoporosis.
Bone loss
Chronic inflammation has been associated with progression of bone loss and micro- architecture deterioration through oxidative stress and excessive production of pro-inflammatory molecules such as tumor necrosis factor-alpha (TNF-alpha).
Various anti-oxidant and anti-inflammatory compounds, such as green tea, alfacalcidol, and soy isoflavones have been suggested suppress TNF-alpha expression.
The researchers noted that certain compounds suggested to inhibit inflammation via suppressing TNF-alpha expression, may have therapeutic value in the prevention and treatment of chronic inflammation-induced bone loss.
In particular green tea (Camellia sinensis), has been suggested to have a wide range of effects on animal and human health due to its anti-oxidant and anti-inflammatory properties.
It has been reported in previous studies to have beneficial effects in various inflammatory conditions, such as inflammatory bowel disease, collagen-induced arthritis and lipopolysaccharide (LPS)-induced gingival inflammation.
The new study investigated the effects of green tea polyphenols and alfacalcidol on bone microstructure and strength along with possible mechanisms in rats with chronic inflammation.
Damage reversal
The researchers reported that both extracted green tea polyphenols and alfacalcidol supplementations reversed LPS-induced changes in bone structure, whilst a combination of both was shown to sustain bone micro-architecture and strength.
In addition green tea polyphenol extract and alfacalcidol were also found to significantly improve femoral strength, and significantly suppress expression of TNF-alpha.
The authors also noted significant interactions in bone mass and strength, the number of bone cells called osteoclasts (cells that break down bone) in leg bone.
Down-regulation
The researchers concluded that present study demonstrates that alfacalcidol administration, green tea polyphenol supplementation and a combination of both significantly down-regulated TNF-alpha expression induced by chronic lipopolysaccharide stimulation.
They stated that the protective impact of green tea polyphenols and alfacalcidol in bone micro-architecture during chronic inflammation may be due to the suppression of TNF-alpha.
According to the authors, the study also shows that the improvement in bone micro-architecture and quality along with the down-regulation bone TNF-alpha expression mechanism further corroborate the anti-inflammatory role of green tea polyphenols and 1-alpha-OH-vitamin D3 (alfacalcidol) in skeletal health – which may reduce the risk of osteoporosis.
They noted that such protective effects on bone micro- architceture are consistent with other antioxidants, for example, soy isoflavones or dried plum polyphenols using the same model of bone deterioration.
Shen and colleagues added that future studies “should address the mechanistic profiles to clarify the preventive role of green tea polyphenol and alfacalcidol in process of bone re-modeling [in] chronic inflammation.”
Source: The Journal of Nutritional Biochemistry
Published online ahead of print, doi: 10.1016/j.jnutbio.2010.05.007
“Protective actions of green tea polyphenols and alfacalcidol on bone microstructure in female rats with chronic inflammation”
Authors: C.L. Shen, J.K. Yeh, C. Samathanam, J.J. Cao, B.J. Stoecker, R.Y. Dagda, M.C. Chyu, J.S. Wang