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Purpose: To establish a method for the preparation of zoledronate liposome and to observe its effect on inducing the apoptosis of rat liver Kupffer cells. Methods: Zoledronate was encapsulated in liposomes, and then the entrapment rate was detected on a spectrophotometer. The prepared Zoledronate liposome (0.01 mg/mL) was injected into the tail vein of SD rats. Three days later, the number of Kupffer cells (CD68 positive) in rat liver tissue was detected by immunohistochemistry. Flow cytometry was used to detect the apoptosis rate of the isolated liver Kupffer cell cultured in vitro. Results: The entrapment rate of Zoledronate was 43.4±7.8%. Immunohistochemistry revealed that the number of Kupffer cells was 19.3±2.1 in PBS group and 5.5±1.7 in Zoledronate liposome group, with a significant difference (P

BACKGROUND The goal of this study was to observe the effect of the apoptosis of Kupffer cells (KCs) selectively induced by zoledronate liposomes following the hepatic ischemia-reperfusion injury (IRI) in the rat liver transplantation model and to explore its mechanisms. MATERIAL AND METHODS The rat liver transplantation model was established using the improved Kamada method. Male Sprague Dawley rats were randomly divided into 3 groups: no liver transplantation or drug treatment (Group A); donor rats were injected with 1 mL normal saline through the tail vein for 3 continuous days before transplantation, and the donor liver was preserved in cold for 2 hours (Group B); donor rats were injected with 1 mL zoledronate liposomes (0.001 mg/mL) through the tail vein for 3 continuous days before transplantation, and the donor liver was preserved in cold for 2 hours (Group C). At 24 hours after transplantation, the receiving rats were sacrificed for sampling. RESULTS Compared with Group C and Group A, the bile secretion flow was dramatically decreased in Group B, whereas the serum liver function index [alanine aminotransferase (ALT), glutamate aminotransferase (AST), and γ-glutamyl transpeptidase (γ-GT)] was significantly increased (P

To investigate the effect and possible mechanisms of Bcl-xL gene on the invasive capacity of human colon cancer cells.HT29 human colorectal carcinoma cell line was transfected by small interfering RNA (siRNA) of Bcl-xL gene. Quantitative real-time (RT)-PCR and Western blot were used to detect the transfection, and soft agar colony culture experiments and Boyden chamber model test were used for cancer cell proliferation and invasion, respectively. Western blot was used to detect the protein changes of urokinase-type plasminogen activator (uPA) in cancer cells.Compared with the control group, the number of soft agar colonies and the number of penetrating membrane cells significantly reduced in the siRNA transfection group, and had dose-dependent characteristics; the uPA protein decreased significantly in the siRNA transfected cells.Bcl-xL gene may play an important role in the invasion of colon cancer cells, and the mechanism may be related to regulation of uPA expression.

Herb-drug interaction strongly limits the clinical utilization of herbs and drugs. Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan. The present study aims to determine the influence of herbal component psoralidin toward the toxicity of irinotecan. In vitro inhibition potential of psoralidin toward the glucuronidation of SN-38 was firstly investigated using human intestinal microsomes incubation system. Dose-dependent inhibition of psoralidin toward SN-38 glucuronidation was observed. Furthermore, Dixon plot showed that the intersection point was located in the second quadrant, indicating the competitive inhibition of psoralidin toward the glucuronidation of SN-38. Through the data fitting using competitive inhibition fitting equation, the inhibition kinetic parameter (K i) was calculated to be 5.8 μM. The translation of these in vitro data into the in vivo situation showed that pre-treatment with psoralidin significantly increased the toxicity of irinotecan, as indicated by the increased body weight loss and more severe colon histology damage. All these data indicated the herb-drug interaction between irinotecan and psoralidin-containing herbs.