Anti-inflammatory potential of ginsenoside Rh1 combined DEX in CIA. (A) After onset of arthritis, CIA mice were randomized in a PBS, DEX (1 mg/kg) treatment or Rh1 (10 mg/kg) combined with DEX (1 mg/kg) treatment protocol. Disease severity was monitored daily. Dots and bars represent mean ± SEM. *P <0.05, **P <0.01 compared with PBS, # P <0.05 compared with DEX. (B) Histopathology of paw joints 10 days post-arthritis onset. HE staining of the metacarpophalangeal joint: a, b, c and d are representative images for blank (normal mice), PBS-, DEX- and Rh1 combined with DEX-treated mice, respectively. The different parameters assessed are 1) influx of inflammatory cells in joint capsule, 2) cartilage destruction, 3) joint cavity narrowing, 4) influx of inflammatory cells in marrow cavities, and 5) and periosteal thickening. (C) Real time PCR was performed in parallel on liver tissues extracts with GR primers. Gene expression of the housekeeping gene GAPDH was used for normalization. *P <0.05, **P <0.01 compared with blank, ##P <0.01 compared with DEX. (D) The blood glucose concentration was determined 6 h after treatment (mice were fasted 18 h before the blood samples were taken). The normal mice were as blank. Values are expressed as means ± SD. *P <0.01 versus blank??; #P <0.01 versus DEX group. (E) Liver samples were taken from the CIA mice after 10 days of treatment. PCR analysis with primers detects the household gene β-actin (loading control) or the gene coding for PEPCK and G6P in the same sample. *P <0.05, **P <0.01 compared with blank, #P <0.05, ##P <0.01 compared with DEX. CIA, collagen-induced arthritis; DEX, dexamethasone; G6P, glucose-6-phosphatase; GR, glucocorticoid receptor; PBS, phosphate-buffered saline; PEPCK, phosphoenolpyruvate carboxykinasee phosphatase.