Green tea protects human osteoblasts from cigarette smoke-induced injury: possible clinical implication

Langenbecks Arch Surg. 2012 Mar;397(3):467-74. doi: 10.1007/s00423-011-0882-8. Epub 2011 Dec 8.

Abstract

Purpose: Recent reports discuss the altered bone homeostasis in cigarette smokers, being a risk factor for osteoporosis and negatively influencing fracture healing. Cigarette smoke is known to induce oxidative stress in the body via an increased production of reactive oxygen species (ROS). These increases in ROS are thought to damage the bone-forming osteoblasts. Naturally occurring polyphenols contained in green tea extract (GTE), e.g., catechins, are known to have anti-oxidative properties. Therefore, the aim of this study was to investigate whether GTE and especially catechins protect primary human osteoblasts from cigarette smoke-induced damage and to identify the underlying mechanisms.

Methods: Primary human osteoblasts were isolated from patients' femur heads. Cigarette smoke medium (CSM) was obtained using a gas-washing bottle and standardized by its optical density (OD(320)) at λ = 320 nm. ROS formation was measured using 2'7'dichlorofluorescein diacetate, and osteoblasts' viability was detected by resazurin conversion.

Results: Co-, pre-, and post-incubation with GTE and catechins significantly reduced ROS formation and thus improved the viability of CSM-treated osteoblasts. Besides GTE's direct radical scavenging properties, pre-incubation with both GTE and catechins protected osteoblasts from CSM-induced damage. Inhibition of the anti-oxidative enzyme HO-1 significantly reduced the protective effect of GTE and catechins emphasizing the key role of this enzyme in GTE anti-oxidative effect.

Conclusions: Our data suggest possible beneficial effects on bone homeostasis, fracture healing, and bone mineral density following a GTE-rich diet or supplementation.

MeSH terms

  • Bone Density
  • Camellia sinensis*
  • Catechin / pharmacology*
  • Dose-Response Relationship, Drug
  • Fracture Healing
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Osteoblasts / drug effects*
  • Osteoporosis
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Smoking / adverse effects*

Substances

  • Reactive Oxygen Species
  • Catechin
  • HMOX1 protein, human
  • Heme Oxygenase-1