Effect and mechanism of sterile Dendrobium officinale nanoparticles on liver injury in mice

  Objective  To explore pharmacological effect and mechanism of sterile Dendrobium officinale nanoparticles (DON) on liver injury.

  Methods  Fifty Kunming mice were randomly divided into a normal control group, model group, low- and high-DON groups (LDON and HDON with gastric gavage of DON at doses of 0.125 and 0.250 g/kg once a day continuously for 7 days), and common Dendrobium officinale powder group (DOP with DOP of 0.250 g/kg). Levels of alkaline phosphatase (ALP), alcohol dehydrogenase (ADH) and total antioxidant capacity (T-AOC) in plasma, the glutathione peroxidase (GPX) activity, glutathione (GSH) and catalase (CAT) contents in liver tissues were detected with kit assay. Cell apoptosis rate in hepatocyte suspension was determined with flow cytometry. Expression of tumor necrosis factor-α (TNF-α) was detected with immunohistochemistry. The expression of B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), caspase-3 and caspase-8 in liver tissues were detected with Western blot.

  Results  Compared with those in the model group, the levels of of serum ALP (31.82 ± 3.35 U/L) and ADH (54.37 ± 2.89 U/mL) was significantly decreased (both P < 0.01) and T-AOC capability (8.30 ± 2.06 U/mL) was improved (P < 0.05) in HDON group; the activity of CAT (68.56 ± 4.07 U/mg), GP_X (523.65 ± 32.67 U/mg) and GSH (26.28 ± 3.98 μmol/g) in liver tissues were increased (all P < 0.01); the apoptosis rate of hepatocytes was significantly decreased (P < 0.01); in liver tissues, the expression of TNF-α was significantly down-regulated (P < 0.01); Bax, caspase-3 and caspase-8 protein expression decreased (both P < 0.01) but bcl-2 (1.13 ± 0.12) protein expression increased (P < 0.01). Compared with those of the DOP group, the improvements in all the indexes of the DON group were more obvious.

  Conclusion  The protective effect of DON on liver injury in mice is significantly better than that of DOP, and the mechanism of the effects may be related to antioxidant damage, inhibited expressions of inflammatory cytokines and reduced liver cell apoptosis.