title: Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model.
abstract: The purpose of this study was to explore the bioavailability, efficacy and molecular mechanisms of green tea polyphenols (GTP) related to preventing bone loss in rats with chronic inflammation. A 2 [placebo vs. lipopolysaccharide (LPS)]×2 (no GTP vs. 0.5% GTP in drinking water) factorial design enabled the evaluation of effects of LPS administration, GTP levels, and LPS×GTP interaction. Urinary GTP components and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were determined by high-pressure liquid chromatography for bioavailability and molecular mechanism, respectively. Efficacy was evaluated by examining changes in femoral mineral content (BMC) and density (BMD) using dual-energy X-ray absorptiometry, and bone turnover biomarkers [osteocalcin (OC) and tartrate-resistant acid phosphatase (TRAP)] using respective ELISA kits. The mRNA expression of tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) in spleen was determined by real-time RT-PCR. Neither LPS administration nor GTP levels affected body weight and femoral bone area throughout the study period. Only GTP supplementation resulted in increased urinary epigallocatechin and epicatechin concentrations. LPS administration led to a decrease in femur BMC and BMD, and serum OC levels, but an increase in serum TRAP, urinary 8-OHdG and spleen mRNA expression of TNF-α and COX-2 levels. GTP supplementation resulted in higher values for femur BMC, BMD and serum OC, but lower values for serum TRAP, urinary 8-OHdG and spleen mRNA expression of TNF-α and COX-2 levels. We conclude that GTP mitigates bone loss in a chronic inflammation-induced bone loss model by reducing oxidative stress-induced damage and inflammation.
authors: Department of Pathology, Texas Tech University Health Sciences Center, Lubbock, TX 79430-9097, USA. leslie.shen@ttuhsc.edu
authors: Chwan-Li
authors: CL
authors: Shen
authors: James K
authors: JK
authors: Yeh
authors: Jay J
authors: JJ
authors: Cao
authors: Owatha L
authors: OL
authors: Tatum
authors: Raul Y
authors: RY
authors: Dagda
authors: Jia-Sheng
authors: JS
authors: Wang
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D001483:Base Sequence; D001682:Biological Availability; D001835:Body Weight / Q000187:drug effects; D001851:Bone Diseases, Metabolic / Q000209:etiology / Q000517:prevention & control*; D016723:Bone Remodeling; D002851:Chromatography, High Pressure Liquid; D002908:Chronic Disease; D051546:Cyclooxygenase 2 / Q000235:genetics; D017931:DNA Primers; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D004195:Disease Models, Animal; D004327:Drinking Behavior / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005419:Flavonoids / Q000493:pharmacokinetics / Q000494:pharmacology*; D007249:Inflammation / Q000150:complications*; D010636:Phenols / Q000493:pharmacokinetics / Q000494:pharmacology*; D059808:Polyphenols; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D013662:Tea / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D017931:DNA Primers; D005419:Flavonoids; D010636:Phenols; D059808:Polyphenols; D012333:RNA, Messenger; D013662:Tea; D014409:Tumor Necrosis Factor-alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D051546:Cyclooxygenase 2; D003849:Deoxyguanosine