RESUMEN
This study aimed to investigate the oxidative neurotoxicity induced by silver nanoparticles (AgNPs) and assess the neuroprotective effects of quercetin against this toxicity. Forty adult male rats were divided into four equal groups: control, AgNPs (50 mg/kg intraperitoneally), quercetin (50 mg/kg orally), and quercetin + AgNPs. After 30 days, blood and brain tissue samples were collected for further studies. AgNP exposure increased lipid peroxidation and decreased glutathione peroxidase, catalase, and superoxide dismutase activities in brain tissue. AgNPs decreased serum acetylcholine esterase activity and γ-aminobutyric acid concentrations. AgNPs upregulated tumor necrosis factor-α, interleukin-1ß, and Bax transcript levels. AgNPs reduced the transcripts of claudin-5, brain-derived neurotrophic factor, paraoxonase, nuclear factor-erythroid factor 2 (Nrf2), and Bcl-2. Histopathologically, AgNPs caused various degenerative changes and neuronal necrosis associated with glial cell reactions. AgNPs increased the immunohistochemical staining of glial fibrillary acidic protein (GFAP) in the cerebrum and cerebellum. Oral treatment with quercetin efficiently counteracted the opposing effects of AgNPs on brain tissue via modulation of tight junction proteins, Nrf2, and paraoxonase, and its positive mechanism in modulating pro-inflammatory cytokines and the downregulation of GFAP expression, and the apoptotic pathway. AgNPs also altered the severity of histopathological lesions and modulated GFAP immunostaining in the examined tissue.
RESUMEN
Gastric ulceration is a multifactorial disease defined as a defect in the gastric wall that extends through the muscularis mucosae into the deeper layers of the wall. The most common cause of gastric ulceration is alcohol consumption. In the current study, rats were gavaged by ethanol to investigate the protective (before ethanol) and curative (after ethanol) ability of Commiphora myrrh (myrrh) oil and extract against gastric ulcer oxidative alterations induced by ethanol. Myrrh significantly improved ulcer index, histomorphology, and periodic acid Schiff (PAS) impaired by ethanol. In addition, myrrh improved the antioxidant potential of gastric mucosa through enhancement of nuclear factor related to erythroid 2 (Nrf2), total glutathione (GSH), reduced GSH, and oxidized glutathione (GSSG), along with significant reduction in malondialdehyde (MDA) levels. Amelioration of gastric oxidative stress by myrrh enables gastric mucosa to counteract the ethanol's inflammatory and apoptotic processes leading to improved gastric proliferation and healing. Interestingly, myrrh extract showed better protective and curative effects than myrrh oil against gastric ulceration.
RESUMEN
The original publication of this paper contains a mistake. The correct image of figure 3 is shown in this paper.
RESUMEN
Silver nanoparticles (AgNPs) are noble metal nanoparticles, due to their good physicochemical properties, which have been exploited in biological applications. Nanotechnological applications advance very quickly while few literatures assessed the effects of natural products on the risks of nanoparticles in vivo. Thirty male adult rats were enrolled equally into: control, AgNPs (50 mg/kg b.w i.p 3 times/week) and GBE (100 mg/kg b.w daily per os)+AgNPs. After 30 days, the assessment of liver function, antioxidative status, mitochondrial biogenesis, and histopathological analyses were performed. AgNP exposure enhanced the hepatic lipid peroxidation (+ 281.7%) along with a decline in the reduced glutathione (- 58.3%) levels. The apparent hepatic oxidative damage was associated with obvious hepatic dysfunction that was ascertained by alteration of serum liver enzymatic biomarkers, lipid profile, and pathological hepatic lesions. Following AgNP exposure, hepatic silver and calcium contents were increased without changes in the trace element concentrations. Finally, the mRNA transcripts of hepatic PGC-1α, mtTFA, and Nrf2 were downregulated after AgNP exposure. Interestingly, GBE has the ability to alleviate AgNP-induced hepatic damage assessed by augmentation of reduced glutathione level and mitochondrial biogenesis. This study explored the potential protective role of GBE on AgNPs-induced hepatotoxicity via attenuation of oxidative stress, substantial enhancement of cell viability with concomitant mitigating DNA damage, and mitochondrial dysfunction.
