Cholestatic liver disease is recognized by extreme collagen formation and deposition, which is mediated by free radicals. The aim of the current study was to investigate the probable hepatoprotective effects of hydroalcoholic extract of watercress (WC) against oxidative stress and liver injury in bile duct ligation (BDL)‐ induced cholestatic rats. A total of 32 male Wistar rats were divided into four groups; sham control (SC), BDL, SC + hydroalcoholic extract of WC and BDL + hydroalcoholic extract of WC. WC‐treated rats received daily WC 500 mg/kg/day for 10 days. Biochemical tests, hepatic oxidative stress markers, and antioxidant enzymes activity were estimated. Further, liver hydroxyproline content was assayed and histological analysis was made. The BDL model markedly elevated the protein carbonyl (PCO) and hydroxyproline contents and decreased the glutathione peroxidase (GPx) activity. Hydroalcoholic extract of WC significantly decreased the surge in liver PCO and hydroxyproline levels and increased the reduced GPx enzyme activity contents in the hepatic tissue. As determined by hematoxylin and eosin staining, BDL considerably induced hepatocyte necrosis. Moreover, these changes were significantly attenuated by the hydroalcoholic extract of WC treatment. Our data indicate that the hydroalcoholic extract of WC extract attenuated liver damage in BDL rats by decreasing the hydroxyproline content and histopathological indexes. Also, it reduced oxidative stress by preventing the hepatic protein oxidation and enhancing the activity of the GPx enzyme via antioxidative effect and free‐radical scavenging. Our findings suggest that hydroalcoholic extract of WC could be a beneficial new curative agent for cholestatic liver damage.

Neural stem cell (NSC) culture is a remarkable tool to investigate the potential therapeutic benefits of drugs in neurological diseases. The purpose of this study was to determine the effect of melatonin on proliferation and differentiation of NSCs in vitro. NSCs were isolated and expanded from mouse embryonic E14 cortex, and the effect of various concentrations of melatonin (0.05, 0.1, 0.5, 1, 5 and 10 μM) on NSC proliferation was assessed by MTT and neurosphere assay. Results showed that melatonin significantly increased NSC viability and NSC proliferation in a dose-dependent manner, in comparison to controls. Similarly, neurosphere formation frequency and cell counts increased significantly with increasing melatonin concentrations and reached its peak at 0.5 μM, in comparison to controls. Moreover, NSCs treated with either low (0.05 µM) or high concentrations (5 µM) of melatonin showed that the mean percentage of glial fibrillary acidic protein (GFAP) positive cells were not significantly different in PDGF or melatonin at 5 μM, in comparison to controls. However, low melatonin concentrations (0.05 µM) showed a slight significant increase in comparison to controls and PDGF. On the other hand, both concentrations of melatonin treatment significantly increased the percentage of myelin basic protein (MBP) positive cells (oligodendrocytes), in comparison to controls and to PDGF. Our results demonstrated, for the first time, that melatonin increased oligodendrocyte differentiation from NSCs. These results suggest that melatonin might have a potential therapeutic effect for some neurological diseases that involve oligodendrocyte and myelin pathologies.

Context:Stachys pilifera Benth (Lamiaceae) has long been used to treat infectious diseases, respiratory and rheumatoid disorders in Iranian folk medicine. Antitumor and antioxidant activity of the plant have been reported.Objective: The study was designed to assess the hepatoprotective activity of ethanol extract of Stachys pilifera in carbon tetrachloride (CCl4)-induced hepatotoxicity in rats.Materials and methods: The rats were randomly divided into six equal groups (n = 7). Group I was treated with normal saline; Group II received CCl4 (1 mL/kg. i.p., twice a week) for 60 consecutive days; Groups III, IV and V were given CCl4 plus Stachys pilifera (100, 200 and 400 mg/kg/d,p.o.); Group VI received the extract (400 mg/kg/d, p.o.). Histopathological analysis and measurement of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), malondialdehyde (MDA), total protein (TP) and albumin (ALB) were performed.Results: CCl4 caused a significant increase in the serum levels of AST, ALT, ALP and MDA as well as decreased ALB, and TP serum levels (p < 0.001). The extract (200 and 400 mg/kg/d) significantly normalized the CCl4-elevated levels of ALT, AST, ALP and MDA (p < 0.001). The extract (200 and 400 mg/kg/d) also increased the serum levels of TP compared to CCl4 group (p< 0.01). The extract (200 and 400 mg/kg/d) also decreased the histological injuries (inflammation and fatty degeneration) by CCl4.Discussion: The results revealed that the Stachys pilifera extract could provide considerable protection against CCl4 hepatotoxicity in rats that may be related to its antioxidant properties.

Stachys pilifera (S. pilifera) Benth (Lamiaceae) is used in traditional medicine to treat a variety of diseases. Despite some reports on the antitumor effects of some species of this genus, anticancer activity of S. pilifera has not been yet reported. Here, we examined the cytotoxic effect and cell death mechanisms of methanolic extract of S. pilifera and its alkaloid and terpenoid fractions on the HT-29 colorectal cell line. HT-29 cells were cultivated and then incubated in the methanolic extract of S. pilifera and its fractions at various concentrations for 24 h. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Morphology of cells was evaluated by contrast microscopy. Furthermore, effects of the tested extract and fractions were tested on some regulators of cell death and proliferation such as caspase-8, caspase-9, nuclear factor-κB (NF-κB), and nitric oxide (NO). Cisplatin was used as positive control. The estimated IC50 values of the methanolic extract, alkaloid and terpenoid fractions, and cisplatin against HT29 cell after 24 h were determined to be 612, 48.12, 46.44, and 4.02 μg/mL, respectively. Morphological changes such as plasma membrane blebbing, cell size reduction, and apoptotic bodies were observed in cells faced with the extract and fractions. S. pilifera extract and its fractions induced apoptosis through inhibition of NF-κB, NO, and activation of caspase-8 and caspase-9. Data showed considerable cytotoxic and antiproliferative effects of S. plifera on colorectal cell line through induction of apoptosis. These findings provide a basis for the therapeutic potential of S. pilfera in the treatment of colon cancer.

Background and purpose: Pulmonary fibrosis is a chronic disease of the lungs caused by inflammation, species of reactive oxygen, and immune defects. Antioxidant properties of Nasturtium officinale has been reported in some studies. Therefore, the objective of the current study was to evaluate the effect of ethanolic extract of Nasturtium officinale (EENO) on bleomycin (BLM)-induced lung fibrosis in rats. Experimental approach: Forty adult male Wistar rats (180-220 g) were randomly divided into 5 experimental groups. Normal control, BLM control received a single dose of BLM (6 IU/kg) intratracheally only on the first day, EENO + BLM group received EENO (500 mg/kg) one week before intratracheal BLM instillation and two weeks afterward, BLM + EENO group and BML + vitamin E group received EENO (500 mg/kg) and vitamin E (500 mg/kg) half-hour after BLM installation, respectively. The animals were sacrificed on day 22. Change in body weight, lung index, serum level of malondialdehyde (MDA) and nitric oxide (NO) metabolite, lung tissue hydroxyproline content and lung pathology were assessed. Findings/Results: Pre- or post-treatment with EENO attenuated pulmonary fibrosis as evidenced by normalized lung index, improved histological changes and inhibited collagen deposition (hydroxyproline) in the animal lung. EENO also decreased MDA and NO metabolite release in comparison to the BLM control. vitamin E (500 mg/ kg) also significantly inhibited the BLM-induced lung toxicity. Conclusions and implications: EENO can prevent BLM-induced lung fibrosis in rats via antioxidant activities. However, more studies are needed to elicit the exact mechanism of this effect.