The aim of the current study was to investigate the protective effect of naringin on bleomycin-induced pulmonary fibrosis in rats. Twenty-four Wistar rats randomly divided into four groups (control, bleomycin alone, bleomycin + naringin 40, and bleomycin + naringin 80) were used. Rats were administered a single dose of bleomycin (5 mg/kg; via the tracheal cannula) alone or followed by either naringin 40 mg/kg (orally) or naringin 80 mg/kg (orally) or water (1 mL, orally) for 14 days. Rats and lung tissue were weighed to determine the lung index. TNF-α and IL-1β levels, hydroxyproline content, and malondialdehyde (MDA) levels were assayed. Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were determined. Tissue sections were stained with hematoxylin-eosin, Masson's trichrome, and 0.1% toluidine blue. TNF-α, IL-1β, and MDA levels and hydroxyproline content significantly increased (p < 0.01) and GPx and SOD activities significantly decreased in bleomycin group (p < 0.01). Naringin at a dose of 80 mg/kg body weight significantly decreased TNF-α and IL-1β activity, hydroxyproline content, and MDA level (p < 0.01) and increased GPx and SOD activities (p < 0.05). Histological evidence supported the results. These results show that naringin has the potential of reducing the toxic effects of bleomycin and may provide supportive therapy for conventional treatment methods for idiopathic pulmonary fibrosis.

Context: Morus nigra L. (Moraceae) has various uses in traditional medicine. However, the effect of M. nigra on cognitive impairment has not been investigated yet. Objective: The objective of this study is to determine the phenolic acid content and DNA damage protection potential of M. nigra leaf extract and to investigate the extract effect on cognitive impairment and oxidative stress in aging mice. Materials and methods: Phenolic acid content was determined by quantitative chromatographic analysis. DNA damage protection potential was evaluated on pBR322 plasmid DNA. Thirty-two Balb-C mice were randomly divided into four groups (control, D-galactose, D-galactose + M. nigra 50, and D-galactose + M. nigra 100). Mice were administered D-galactose (100 mg/kg, subcutaneous) and M. nigra (50 or 100 mg/kg, orally) daily for 8 weeks. Behavioral responses were evaluated with Morris water maze. Activities of antioxidant enzymes and levels of malondialdehyde (MDA) were assayed in serum, brain, and liver. Results: In extract, vanillic (632.093 mg/g) and chlorogenic acids (555.0 mg/g) were determined. The extract between 0.02 and 0.05 mg/mL effectively protected all DNA bands against the hazardous effect of UV and H 2 O 2 . Morus nigra significantly improved learning dysfunctions (p 50.01), increased memory retention (p50.01), reduced MDA levels (p50.05), and elevated SOD, GPx, and CAT activities (p50.05) compared with the D-galactose group. Discussion and conclusion: These results show that M. nigra has the potential in improving cognitive deficits in mice and that M. nigra may be useful to suppress aging, partially due to its scavenging activity of free radicals and high antioxidant capacity. ARTICLE HISTORY

OBJECTIVE: The aims of this study were to investigate the protective effect of quercetin on changes in recognition memory as assessed by the novel object recognition (NOR) test, as well as on changes in the oxidative stress levels in the hippocampus and prefrontal cortex, produced in a model of memory impairment in schizophrenia induced by administration of a subanesthetic dose of ketamine. METHODS: A total of 40 Balb-C mice were randomly divided into five groups (Corn oil + Saline, Quercetin 50 + Saline, Corn oil + Ketamine, Quercetin 25 + Ketamine, Quercetin 50 + Ketamine). Corn oil and Quercetin (25 or 50 mg/kg/day) was given by orogastric gavage once daily for 21 days. Corn oil was chosen as the vehicle and administered at the same volume as quercetin. Ketamine was injected at a dose of 25 mg/kg intraperitoneally (i.p.) for a period of 7 days starting from the 15th day. Behavioural responses were evaluated with the NOR test. The activity levels of antioxidant enzymes and levels of malondialdehyde (MDA) were assayed in the prefrontal cortex and hippocampus. RESULTS: The time of exploration of the novel object was longer than T F (time to explore the familiar object) in the Corn oil + Saline and Quercetin 50 + Saline groups in NOR Test-1 (p < .05). The discrimination ratios of the Quercetin 50 + Ketamine and Corn oil + Ketamine groups were significantly lower than that of the Quercetin 50 + Saline group (p < .05). The discrimination ratios of the Quercetin 50 + Ketamine and Corn oil + Saline groups were significantly lower than that of the Quercetin 50 + Saline group (p < .05). The time of exploration of the novel object was longer than T F in the Corn oil + Saline and Quercetin 50 + Ketamine groups in NOR Test-2 (p < .05). The discrimination ratios of the Corn oil + Ketamine and Quercetin 25 + Ketamine groups were significantly lower than those of the Quercetin 50 + Ketamine group (p < .05). Quercetin at 50 mg/kg reduced the MDA levels and elevated the SOD and GPx activity compared to the Corn oil + Ketamine group. CONCLUSION: These results show that quercetin has the potential to improve cognitive deficits in mice and that quercetin may be useful for treating the symptoms of schizophrenia, partially due to its ability to scavenge free radicals and its high antioxidant capacity.

No abstract

No abstract

IntroductionAlzheimer disease (AD) is neurodegenerative disease, characterized by the gradual deterioration of memory and other cognitive functions. Increase in age is a major risk factor for this disease and the prevalence of AD has increased worldwide as the elderly population of the world is increasing (1). The neuropathological hallmarks of AD brains are amyloid beta fibrils in senile plaques, neurofibrillary tangles, and neuronal loss (2). The etiopathogenesis of AD is multifactorial and it is suggested that oxidative stress has a significant role in the beginning and progression of this disease, yet the sources of free radicals and the mechanisms disrupting the redox balance remain elusive (3-5).D-Galactose is a reducing sugar found in the body. When it is present at higher levels than normal, it can be converted to galactitol by galactose oxidase, resulting in the generation of oxygen-derived free radicals (6). Chronic systemic exposure to D-galactose induces aging-related changes such as corruption of spatial learning, memory loss, neurodegeneration, and diminishing activities of antioxidant enzymes and increased production of free radicals (7-9).Capparis spinosa L. is a long-lasting shrubby plant that belongs to the family Capparidaceae and grows naturally throughout the world, especially widely in the Mediterranean basin. It has been used since ancient times for aromatic properties in cooking, and besides its use as flavoring, C. spinosa has also been used as a traditional herbal medicine for its antihypertensive, poultice, tonic, and diuretic characteristics (10). This plant has been investigated for several pharmacological effects. The bud extract of C. spinosa inhibits the replication of herpes simplex virus type 2 and upregulates the expression of proinflammatory cytokines (11). It was demonstrated that the methanol extracts of C. spinosa flowering buds have antiallergic effectiveness (12), and the lyophilized extract of C. spinosa buds shows in vitro antioxidant effectiveness Background/aim: To determine the phenolic acid levels and DNA damage protection potential of Capparis spinosa L. seed extract and to investigate the effect of the extract on cognitive impairment and oxidative stress in an Alzheimer disease mice model. Materials and methods:Thirty BALB/c mice divided into 5 groups (control, D-galactose, D-galactose + C. spinosa 50, D-galactose + C. spinosa 100, D-galactose + C. spinosa 200) were used. Mice were administered an injection of D-galactose (100 mg/kg, subcutaneous) and orally administered C. spinosa (50, 100, or 200 mg/kg) daily for 8 weeks.Results: Syringic acid was detected and the total amount was 204.629 µg/g. Addition of 0.05 mg/mL C. spinosa extract provided significant protection against the damage of DNA bands. C. spinosa attenuated D-galactose-induced learning dysfunctions in mice and significantly increased memory retention. Malondialdehyde (MDA) levels increased and superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities decreased in the D-...

Cherry fruit (Prunus avium L.) is cultivated in lands located in the temperate region of the world, and Turkey, United States of America and Iran are major producers of it in the world (Perez, Ferreira, & Minor, 2017). Based on the Turkish Statistical Institute data, Turkey's sweet cherry production was 639 534 tons in 2018 (TUIK, 2018). As a country, it provides 26% of cherry production of the world, which makes it one of the leading exporter in the world (Anonymous, 2019). Although cherry is mostly consumed in fresh form, it can be consumed in frozen, canned, juice, wine, brine, and dried forms (Perez et al., 2017). The decoction or infusion of its stem has been used for many years in folk medicine as a renal stone reliever, diuretic, anti-inflammatory, and antihypertensive agent (Hooman, Mojab, Nickavar, & Pouryousefi-Kermani, 2009). Due to their high and easy availability and better biodegradability, there has been interest in natural plant products that can substitute with synthetic drugs (Kalemba & Kunicka, 2003). The studies on the phenolic compounds show a contrary relationship between chronic disease risk and polyphenolic rich diet, and thus, they have positive effects on human health. The plant defense system against various stresses produces them as the secondary metabolites (Carocho & Ferreira, 2013). They have antioxidant properties that can end the propagation of free radical reactions in the biological systems

No abstract