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Background: Picroside II (PII), an iridoid glycoside extracted from the rhizomes and stems of the genus Picroside, exhibits pronounced hepatoprotective properties. Pre-administration of PII protects against acute liver injury caused by D-galactosamine (D-Gal), carbon tetrachloride (CCl4), and acetaminophen (APAP). This study aimed to elucidate the ramifications of PII administration subsequent to the initiation of acute hepatic injury. Methods: Exploring the role of PII treatment in APAP-treated cell and rat models and in D-Gal and CCl4-treated rat models. Results: In rats, APAP treatment increased serum aspartate transaminase, alanine transaminase, and alkaline phosphatase levels and decreased glutathione activity and the fluidity of the liver mitochondrial membrane. In L-02 cells, APAP exposure resulted in a decrement in membrane potential, an augmentation in the liberation of reactive oxygen species, and an acceleration of apoptotic processes. Moreover, PII pre-administration protected against D-Gal-induced acute hepatic injury and CCl4-induced chronic hepatic injury in rodent models, whereas PII administration post-injury aggravated CCl4-induced chronic hepatic injury. Conclusions: Our results suggest that the effects of PII depend on the hepatic physiological or pathological state at the time of intervention. While PII possesses the potential to avert drug-induced acute hepatic injury through the mitigation of oxidative stress, its administration post-injury may exacerbate the hepatic damage, underscoring the critical importance of timing in therapeutic interventions.
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Objective To evaluate the effects of B7-H3 gene transfection on 18F-FDG uptake and 18F-FLT uptake in prostate cancer cells.Methods The absorption (A) values of untransfected prostate cancer(RM1) cells and B7-H3 gene-transfected RM1 (RM1-B7-H3) cells were detected at different culturing time points (0.5,1,2,3,4 and 5 d) with cell counting kit-8 (CCK-8) test.Cell cycle phase distribution of RM1 and RM1-B7-H3 cells was measured with flow cytometry.18F-FDG uptake of RM1 and RM1-B7-H3 cells was measured with γcounter and calculated under different conditions:5× 104-5× 106 cells; 0-11.0 mmol/L glucose; 20-120 min incubation in 37 ℃.18F-FLT uptake of RM1 and RM1-B7-H3 cells was measured in 1×106 cells under incubation for 100 min at 37 ℃.After administering anti-B7-H3 monoclonal antibody 4H7,18F-FDG uptake of RM1-B7-H3 cells was measured.The data were analyzed using one-way analysis of variance and two-sample t test.Results The A values of RM1-B7-H3 cells after being incubated for 1,2 and 3 d were higher than those of RM1 cells(1.59±0.23,2.26±0.15 and 2.01±0.60 vs 1.22±0.14,1.10± 0.09 and 1.04±0.15,t=3.923,19.228,4.467,all P＜0.01).There was no statistical significance between the 2 groups at other time points (t=-0.094,0.858,2.000,all P＞0.05).The ratios of RM1-B7-H3 cells in G1,S and G2/M phases were(32.96±2.56) ％,(39.11 ±2.57) ％ and (27.94±0.21) ％,respectively.The ratio of S phase in RM1-B7-H3 cells was higher than that in RM1 cells ((32.76±1.90)％,t=3.442,P＜ 0.05).18F-FDG uptake of the both cell lines decreased with the increase of glucose concentrations,while the uptake went up with the increase of cell number and incubation time.With the cell number of 1.0× 106,incubation time of 100 min and temperature of 37 ℃,the 18F-FDG uptake of RM1-B7-H3 and RM1 cells was (55.07±3.99)％ vs (44.16±3.60)％ (t=4.977,P＜0.01) ; and 18F-FLT uptake of RM1-B7-H3 and RM1 cells was (5.25±0.81)％ vs (3.33±0.64)％ (t=4.567,P＜0.01).After treated with antibody 4H7,18F-FDG uptake of RM1-B7-H3 cells ((45.36±2.92) ％) was lower than that of untreated group (F=10.001,P＜ 0.01).Conclusion B7-H3 gene transfection may promote the metabolism and proliferation of prostate cancer cells,and thereby increase the 18F-FDG uptake and 18F-FLT uptake.
