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Background: We aimed to study the beneficial property of chrysin (CHR) by targeting its antioxidant and anti-inflammatory effects on nephrotoxicity induced by sodium arsenite (SA)., Materials & Methods: We have used the 35 male Wistar rats in five equal groups (n = 7). Normal saline in (5 ml/kg; p.o.; 21 days) was given to the control group. Sodium arsenite (10 mg/kg; p.o.; 14 days) was given to the SA group. CHR (25, 50 and 100 mg/kg; p.o.; 21 days) and SA (10 mg/kg; p.o.; 14 days from the 7th day of the experiment) was given to the SA + CHR 25, 50 and 100 groups. On the 22nd day of the experiment, the animals' bloods and kidneys were taken, and then we have performed functional, biochemical and histological assessment., Results: CHR pre- and alongside administration (more potently at dose of 100 mg/kg) with SA reduced the SA-induced alterations in serum creatinine and blood urine nitrogen levels. Increased levels of protein carbonyl, myeloperoxidase, malondialdehyde and nitric oxide in kidney tissue were decreased by CHR treatment. CHR administration increased the levels of glutathione and activities of glutathione peroxidase, catalase and superoxide dismutase in renal tissue. Moreover, treatment with CHR reduced the levels of inflammatory mediators including interleukin 1 beta and tumor necrosis factor alpha in renal tissue. The renal histological lesions induced SA were mitigated by CHR treatment in dose dependent manner., Conclusion: The results of present study suggested that administration of CHR before and alongside with SA attenuated the renal toxic effects of SA via antioxidative stress and anti-inflammatory effects., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Epileptic seizures are associated with the release of potentially neurotoxic amount of glutamate, which results in the over-production of free radicals and inflammatory factors, and induction of neuronal cell death. Current study evaluated the effect of tannic acid (TA) on Kainic acid (KA)-induced seizures in mice. Methods: Mice were divided into the six groups. Group I was administrated with normal saline (NS; 1 mL/kg, intraperitoneally (i.p.)), Group II was injected with KA (15 mg/kg, i.p.), Groups III was treated with diazepam (DZ; 20 mg/kg, i.p.) and KA (15 mg/kg, i.p.), Groups IV-VI were treated with TA (25, 50 and 100 mg/kg, i.p.) and KA (15 mg/kg, i.p.). Animals received all treatments 30 min before injection of KA. After the injection of KA, mice were observed for seizure (latency, activity and duration) and mortality for 2 h. In the brain tissue, oxidative stress, apoptosis, and inflammatory markers were evaluated in addition to the determination of histological alterations in the CA1 molecular layer of hippocampus. Results: T reatment with TA significantly increased seizure latency and decreased seizure duration and activity, but could not significantly decrease mice mortality. This effect was associated with the reduction of oxidative stress, inflammation, and apoptosis. Furthermore, treatment with TA significantly improved KA-induced pyramidal cell loss and change in the arrangement of CA1 molecular layer. Conclusions: Tannic acid may be useful in the control of epileptic seizures through regulating oxidative stress, inflammation and apoptosis. [ABSTRACT FROM AUTHOR]

Background: Di-(2-ethylhexyl) phthalate (DEHP) is a well-known endocrine-disrupting compound inducing degeneration of testes. Gallic acid (GA) is a polyphenol with various pharmacological properties, including antioxidant and anti-inflammatory effects. Purpose: This research evaluated effects of different doses of GA on DEHP-induced testicular injury in adult mice. Research Design: Male mice were randomly divided into five groups and treated with agents for two weeks; group (I) received normal saline and corn oil (5 mL/kg/day, p. o.), group (II) received DEHP (2 g/kg/day, dissolved in corn oil, p. o.), groups (III, IV, and V) received DEHP + GA (25, 50, and 100 mg/kg/day, p. o.). Body and testes weights, serum testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels were evaluated. The number of sperms and sperm motility and viability were analyzed in the cauda epididymis. Histological changes, oxidative/nitrosative stress markers, and inflammatory cytokines levels were examined in testes. Results: Body and testes weights, the number of spermatogonia, primary spermatocyte and early spermatid, and late spermatid and sperm vitality, and progressive motility were significantly reduced in mice exposed to DEHP. Serum testosterone level decreased and serum LH and FSH levels increased in DEHP-exposed mice. These alterations were associated with the increased oxidative stress level and inflammatory responses in testicular tissue. Treatment with GA (50 and 100 mg/kg/day) attenuated DEHP-induced alterations in oxidative stress markers and inflammatory cytokines and reversed abnormality in sperm characteristic and number, tissue structure, and serum hormones levels. Conclusions: Results indicated that GA might be a promising agent against male gonadal toxicity induced by endocrine disrupting chemicals including DEHP. [ABSTRACT FROM AUTHOR]

The current investigation was considered to evaluate the beneficial effects of gentisic acid (GA) on gentamicin (GEN)-induced nephrotoxicity in rat kidneys through assessment of oxidative stress, inflammatory cytokines, and histopathological changes. Rats were split into five equal groups. Rats were treated with GA (25, 50, and 100 mg/kg/day, p.o.) for 14 consecutive days and GEN (100 mg/kg, i.p.) was administrated from day 8 to day 14 of the experiment. On the 15th day, blood samples were collected to determine neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), blood urea nitrogen (BUN), and creatinine (Cr) levels. Malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β), and nitric oxide (NO) levels and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were assessed in the renal tissue. Histopathological evaluations were done to confirm the biochemical results. GEN increased the levels of NGAL, KIM-1, BUN, and Cr in serum as well as MDA, NO, GSH, TNF-α, and IL-1β in renal tissue. Moreover, GEN administration reduced the activity of CAT, SOD, and GPx in renal tissue. Nonetheless, the administration of GA before and alongside GEN mitigated these deleterious effects. In conclusion, GA has a beneficial effect on biochemical, inflammatory, and oxidative stress indices against GEN-induced nephrotoxicity. • GEN induces oxidative, inflammatory, and morphological injuries in kidney tissue. • GA, exert different pharmacological activities such as anti-inflammatory, and antioxidant effects. • GA improves GEN-induced alternations in oxidative and inflammatory parameters in kidney tissue. • GA attenuated the histopathological lesions induced by GEN in kidney tissue. • GA can be used as protective agent in kidney injuries induced by GEN. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is the most common autoimmune disease. Progressive depletion of the brain and spinal cord tissue appears at the onset of the disease. Several studies have shown the increased size of the ventricles of the brain and decreases in the area of the corpus callosum and the width of the brain. Other important symptoms of this disease are cognitive, learning, and memory disorders. Aim: The aim of this study was to compare morphometric, histological, and functional changes in the demyelination model in both sexes. Materials and methods: In this experimental study, male and female Wistar rats were studied in four experimental groups. Demyelination was induced by the injection of ethidium bromide in the ventricular region. The chronic effect of demyelination on spatial memory, movement, and coordination was investigated using the Morris Water Maze (MWM), and clinical and balance beam tests, respectively. Myelin degradation, cell death and neurogenesis were estimated using Luxol Fast Blue staining and immunohistochemistry (Caspase‐3 and Nestin markers). In addition, morphometric findings were recorded for the brain and hippocampus (weight, volume, length, width). Result: Demyelination increased the time and distance index and decreased the residence time in the target quarter in the water maze test (p <.001). It also increases the neuromuscular and modified neurological severity score (p <.01). Demyelination increases caspase‐3 (p <.05) expression and decreases Nestin expression (p <.001), which are directly related to the extent of damage. Conclusion: This study showed an interaction between hippocampal structural and functional networks in explaining spatial learning and memory in the early stages of MS. [ABSTRACT FROM AUTHOR]

Lead (Pb) is a highly poisonous environmental pollutant that can induce cognitive decline. Chrysin, a natural flavonoid compound, has anti-oxidative, anti-inflammatory, and neuroprotective properties in different neurodegenerative disorders. The present study was designed to examine the putative effects of chrysin against Pb-induced cognitive impairment and the possible involved mechanisms. Adult male Wistar rats were exposed to Pb acetate (500 ppm in standard drinking water) either alone or in combination with daily oral administration of chrysin (30 mg/kg) for eight consecutive weeks. During the eight-week period of the study, the cognitive capacity of the rats was evaluated by employing both novel object recognition and passive avoidance tests. On day 56, hippocampal synaptic plasticity (long-term potentiation; LTP) was recorded in perforant path-dentate gyrus (PP-DG) synapses to assess field excitatory postsynaptic potentials (fEPSPs) slope and population spike (PS) amplitude. Subsequently, pro- and anti-inflammatory cytokines and histological changes were evaluated in the cerebral cortex and hippocampus of the rats. Moreover, Pb levels in blood and brain tissues were assessed. The results showed that Pb exposure causes cognitive decline, inhibition of hippocampal LTP induction, imbalance of pro- and anti-inflammatory cytokines, enhancement of Pb levels in blood and brain tissues, and neuronal loss. However, chrysin treatment improved cognitive dysfunction, ameliorated hippocampal LTP impairment, modulated inflammatory status, reduced Pb concentration, and prevented neuronal loss in the Pb-exposed rats. The results suggest that chrysin alleviates Pb-induced cognitive deficit, possibly through mitigation of hippocampal synaptic dysfunction, modulation of inflammatory status, reduction of Pb concentration, and prevention of neuronal loss. [Display omitted] • Chrysin improved lead-induced cognitive decline in rats. • Chrysin ameliorated hippocampal synaptic plasticity impairment in lead-exposed rats. • Chrysin modulated inflammation status in lead-exposed rats. • Chrysin alleviated accumulation of lead in blood and neuronal tissues of rats. • Chrysin protected lead-induced neuronal loss in rats. [ABSTRACT FROM AUTHOR]

Asthma is a chronic inflammatory airway disease associated with the airway narrowing and obstruction. Sinapic acid (SA), a hydroxycinnamic acid, possesses various pharmacological properties including antioxidant and anti-inflammatory activity. This research evaluated effects of different doses of SA on murine model of ovalbumin (OVA)-induced allergic asthma. Allergic asthma induced by sensitizing mice on days 1 and 14 by intraperitoneal injection of OVA. After initial sensitization, between days 21 and 23, mice were challenged for 30 min with an aerosol of 1 % (wt/vol) OVA. Treatment with dexamethasone (3 mg/kg) or SA (25, 50 or 100 mg/kg) were done by oral gavage on days 15–23. Inflammatory cells infiltration and interferon-γ (IFN-γ), interlukin-4 (IL-4), IL-5 and IL-13 levels were evaluated in the bronchoalveolar lavage fluid (BALF). Serum total and OVA-specific immunoglobulin E (IgE) and lung tissue nitric oxide (NO) levels were measured. Histological changes in lung tissue were examined by staining with hematoxylin and eosin (H&E) for cell infiltration, periodic acid-Schiff (PAS) for mucus production and Masson's trichrome for collagen deposition. Treatment with SA significantly inhibited inflammatory cell infiltration, enhanced IFN-γ level and decreased IL-4, IL-5 and IL-13 levels in BALF. Serum total and OVA-specific IgE levels and NO level in lung tissue were significantly reduced by SA. Histological examination demonstrated that SA significantly attenuated inflammatory cell infiltration and mucus-producing cells in the lung. These data suggest that SA may be a new therapeutic potential to treat allergic asthma through suppressing T-helper 2 immune responses. [ABSTRACT FROM AUTHOR]

Arsenic as a one of the most important toxic metals could induce hepatotoxicity. Previous reports revealed the significance of oxidative stress in promoting of arsenic-induced liver toxicity. The aim of the present investigation is to evaluate the effect of chrysin (CHR), a natural flavonoid with potent antioxidant activity, against sodium arsenite (SA)-induced hepatotoxicity. Thirty male Wistar rats were divided into four groups: Group 1: received normal saline (2 ml/kg/day, orally for 21 days), Group 2: received SA (10 mg/kg/day, orally for 14 days), Group 3, 4 and 5: received CHR (25, 50 and 100 mg/kg/day, respectively, orally for 21 days) and SA (10 mg/kg/day, orally for 14 days) from the 7th day. Serum levels of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase were evaluated. Moreover, liver glutathione peroxidase and myeloperoxidase activity as well as levels of protein carbonylation, malondialdehyde, glutathione, catalase, nitric oxide, superoxide dismutase, tumor necrosis factor-α and interleukin-1β were evaluated. Moreover, histological evaluation was done. Our results revealed that treatment with CHR (more potentially at the dose of 100 mg/kg/day) before and alongside with SA significantly mitigated the SA-induced hepatotoxicity. Also, the hepatoprotective effect of CHR was verified by the histological evaluation of the liver. The results of current study demonstrated that CHR (100 mg/kg/day) could mitigate the oxidative stress and inflammation induced by SA in liver tissue. Unlabelled Image [ABSTRACT FROM AUTHOR]