---

Background and purpose: Acetaminophen is a routine analgesic and antipyretic agent that in overdose causes liver and kidney necrosis in both humans and animals. The cress (Lepidium sativum L.) contains flavonoid, alkaloid, and antioxidant components. In this study we investigated the hepatic protection of the hydroethanolic extract of cress against hepatotoxicity due to acetaminophen. Materials and methods: Forty-two rats were randomly divided into six groups. The first (control) and second (test without treatment) groups were administered the solvent of drug in the morning (08:00) and evening (16:00) on days 1 and 2 but, the third, fourth, and fifth groups received 200, 500, and 1000 mg/kg b.w of the extract of the cress, respectively. The sixth group (positive control) received 200 mg/kg b.w silymarin. Then all groups, except the control group, received 400 mg/kg acetaminophen per os on day 2 (10:00). After 24 hr, all blood samples were collected for determination of GOT (glutamic-oxaloacetic transaminase), GPT (glutamic- pyruvic transaminase), ALP (alkaline phosphatase), malondialdehyde (MDA), and serum antioxidant capacity. Also, a piece of liver was used for determining catalase activity and histopathological studies. For statistical analysis of the data, group means were analyzed with one way ANOVA followed by Tukey’s test for multiple comparisons. Results: Serum GOT, GPT, ALP, and MDA reduced significantly (P< 0.001) in the treated groups with the extract of cress compared to acetaminophen group without treatment. The reduction of GPT and ALP were dose dependent. The serum antioxidant capacity and liver catalase in treated groups with the extract of the cress and silymarin treated group elevated significantly (P< 0.001) compared to the acetaminophen group without treatment. The liver histopathology in rats treated with the extract of cress showed a remarkable reduction of lymphocyte infiltration compared with rats without treatment (group two). Conclusion: These results demonstrate that the extract of the cress have protection effect against hepatotoxicity due to acetaminophen.

---

Background and purpose: Vascular calcification is an important factor in pathogenesis of atherosclerosis. Studies have shown that alkaline phosphatase increases vascular calcification. Here we investigated the effect of gallic acid on alkaline phosphatase gene expression in vascular smooth muscle cells (VSMCs). Materials and methods: In this experimental study humans aorta VSMCs were incubated with beta glycerol phosphate as calcification-inducing media. Then these cells were treated with 160, 180 and 200 µMol concentration of gallic acid for 24h, 48h and 72h. The total RNA was extracted and cDNA was synthesized and then alkaline phosphatase expression was measured by real time PCR. Alkaline phosphatase specific activity was measured by spectrophotometry. Results: Overall, 160, 180 and 200 µMol concentration of gallic acid decreased alkaline phosphatase gene expression in vascular smooth muscle cell by 1.98, 2.03, and 3.16 folds, respectively after 72h compared with the control group. The alkaline phosphatase specific activity also decreased compared to that of the control group. Conclusion: Our results showed that gallic acid decreased the expression and activity of alkaline phosphatase suggesting that this antioxidant compound may attenuate vascular calcification.

---

Background and purpose: Interleukin-6 (IL-6) causes the progression of prostate cancer through pSTAT3, pERK1/2, and pAKT cell signaling proteins. Quercetin, an herbal antioxidant, has anti-tumor effect. The aim of this study was to evaluate the effects of quercetin on IL-6 gene expression, and the above cellular signaling proteins in PC3 prostate cancer cells.

Materials and methods: In this experimental study, PC3 cells were treated with different concentrations of quercetin at 0, 10, 50, and 100 μM.  Then, IL-6 concentration was determined in cell culture media. Also, total RNA and the cellular signaling proteins aforementioned were extracted from PC3 and used for determining IL-6 gene expression by quantitative real-time RT-PCR and western blot analysis, respectively.

Results: The quercetin IC₅₀ for PC3 prostate cancer cells was 100 μM. Elevation of quercetin concentration in cell culture media increased the IL-6 gene expression and protein synthesis. At 50 and 100 μM of quercetin, IL-6 protein synthesis increased significantly (P<0.05) to 13.36% and 36.86%, respectively, compared to those in control. Furthermore, quercetin suppressed pSTAT3, pERK1/2, and pAKT cell signaling proteins at dose concentrations more than 150 μM.

Conclusion: The effects of quercetin on PC3 cells could have resulted from reduction of pSTAT3, pERK1/2, pAKT, induction of the oxidative stress and generation of reactive oxygen species. Therefore, quercetin can be considered as a useful therapeutic agent in treatment of prostate cancer.