The prolonged use of exogenous glucocorticoids, such as dexamethasone (Dex), is the most prevalent secondary cause of osteoporosis, known as glucocorticoid-induced osteoporosis (GIO). The current study examined the preventative and synergistic effect of aqueous chicory extract (ACE) and ethanolic purslane extract (EPE) on GIO compared with Alendronate (ALN). The phytochemical contents, elemental analysis, antioxidant scavenging activity, and ACE and EPE combination index were evaluated. Rats were randomly divided into control, ACE, EPE, and ACE/EPE MIX groups (100 mg/kg orally), Dex group (received 1.5 mg Dex/kg, Sc), and four treated groups received ACE, EPE, ACE/EPE MIX, and ALN with Dex. The bone mineral density and content, bone index, growth, turnover, and oxidative stress were measured. The molecular analysis of RANK/RANKL/OPG and Nrf2/HO-1 pathways were also evaluated. Dex causes osteoporosis by increasing oxidative stress, decreasing antioxidant markers, reducing bone growth markers (OPG and OCN), and increasing bone turnover and resorption markers (NFATc1, RANKL, ACP, ALP, IL-6, and TNF-α). In contrast, ACE, EPE, and ACE/EPE MIX showed a prophylactic effect against Dex-induced osteoporosis by modulating the measured parameters and the histopathological architecture. In conclusion, ACE/EPE MIX exerts a powerful synergistic effect against GIO by a mode of action different from ALN.

Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs). Four groups of adult male rats (n = 10) were assigned as follows; normal control, ω-3 PUFAs (400 mg/kg) alone, MSG (4 mg/g) alone, and MSG plus ω-3 PUFAs (4 mg/g MSG plus 400 mg/kg ω-3 PUFAs). Biochemical analysis, immunohistochemical, and histological examinations were conducted upon completion of the treatment protocol. Results revealed that MSG significantly increased malondialdehyde, nitric oxide, tumor necrosis factor-α, interleukin 1β, acetylcholinesterase, monoamine oxidase, and caspase-3. However, the MSG-treated group showed a decline in reduced glutathione, catalase, superoxide dismutase, dopamine, and serotonin. In addition, MSG caused histopathological changes in the cortical region which support the biochemical and immunohistochemical analysis. Supplementation of ω-3 PUFAs greatly improved the biochemical, immunohistochemical, and histopathological alterations induced by MSG administration in the brain cortex. Together, these findings revealed a neuroprotective effect of ω-3 PUFAs against MSG-induced toxicity in the brain cortex by attenuating oxidative damage, inflammation, neurochemical perturbations, and apoptosis. Graphical abstract

The excessive intake of monosodium glutamate (MSG) increases its cellular levels in different organs and induces organ toxicity. The current study aims to investigate the metabolic changes and possible causes of hepatic, renal, and cardiac toxicity induced by MSG overconsumption. Thirty adult male rats were randomly allocated into five groups: control, MSG0.8, MSG1, MSG2, and MSG3, which were orally treated with a daily oral dose of saline, 0.8, 1, 2, and 3 g MSG/kg BW, respectively, for eight weeks. The hepatic, renal, and cardiac biochemical markers; lipid profile; glucose; electrolytes; iNOS; α-KGD; oxidative stress; and inflammatory markers were investigated. The histopathological examination of hepatic and renal tissues was also performed. The results revealed MSG-induced hepato-renal and cardiac toxicity, as indicated by the changes in the biochemical markers and tissue architecture of these organs. The toxicity is observed in the form of dyslipidemia, oxidative stress (increased MDA and NO and decreased GSH, SOD, CAT, and GST), and inflammatory responses (increased TNF-α and IL-6). The histopathological changes in liver and kidney architecture confirmed the obtained results. In conclusion, the MSG-induced hepatic, renal, and cardiac toxicity was dose-dependent, and awareness should be raised about the side effects of the overconsumption of MSG.

Exposure to bisphenol A (BPA) contributes to neurological disorders, but the underlying mechanisms are still not completely understood. We studied the neurotoxic effect of BPA and how it promotes inflammation and alteration in the neurotransmission synthesis, release and transmission. This study was also designed to investigate the neuroprotective effect of grape seed proanthocyanidins (GSPE) against BPA-induced neurotoxicity in rats. Rats were equally divided into 4 group with 7 rats in each as follows: control group, BPA group, GSPE + BPA group and GSPE group. Rats were orally treated with their respective doses (50 mg BPA/kg BW and/or 200 mg GSPE/kg BW) daily for 70 days. BPA elicits significant elevation in malondialdehyde (MDA) and nitric oxide (NO) associated with significant reduction in glutathione (GSH), total thiols, glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione-S-transferase (GST). BPA exposure result in increased dopamine and serotonin levels, elevation in acetylcholine esterase (AchE) activity and reduction in Na/K-ATPase and total ATPase activities in the brain. Also, BPA induces upregulation in the gene expression of the inflammatory markers; tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2), and in the tumor suppressor and pro-oxidant p53 protein. The pretreatment with GSPE attenuate or ameliorate all the oxidative and neurotoxic parameters induced by BPA. Our results suggest that GSPE has a promising role in modulating BPA-induced neuroinflammation and neurotoxicity and its antioxidant and free radical scavenging activities may in part be responsible for such effects.