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Introduction: Evidence declared lipopolysaccharide (LPS) initiates inflammatory responses by stimulating the abandon of cytokines, which may perturb organ function. On the other side, it has been suggested Cedrol has potential properties, including anti-inflammatory and anti-oxidative activities. Herein, this study was done to assess the protective effect of Cedrol against LPS-associated heart damage. Methods: Thirty-five rats (200-250 g) were sorted into five groups, including control, LPS, LPS-Cedrol 7.5 mg/kg, LPS-Cedrol 15 mg/kg, and LPS-Cedrol 30 mg/kg groups. Cedrol was administrated through injected intra-peritoneally for two weeks. The heart tissues were removed and malondialdehyde (MDA) as a lipid peroxidation marker, superoxide dismutase (SOD), and catalase (CAT) as antioxidant markers were assessed. Furthermore, the interleukin (IL)-6 level in cardiac tissue was measured and Masson's trichrome methods were employed to appraise cardiac inflammation and fibrosis, respectively. Results: Inflammation induced by LPS was significantly accompanied by myocardial fibrosis which was shown by Masson's trichrome staining (P < 0.001). In addition, LPS administration enhanced the MDA level while it diminished the activity of anti-oxidant markers such as CAT and SOD (P < 0.001 for all cases). In the histological results, Cedrol improved LPS-induced inflammation and cardiac fibrosis (P < 0.01 to P< 0.001). Cedrol also enhanced CAT and SOD activities, whereas declined MDA level in the cardiac tissue (P < 0.01 to P< 0.001). Conclusion: The current findings proposed that the administration of Cedrol exerted a protective role in LPS-associated heart damage by reducing inflammation, cardiac fibrosis, and oxidative stress. [ABSTRACT FROM AUTHOR]

During the elderly, hippocampal neurogenesis and synaptogenesis reduce and dark neurons (DNs) increase, leading to cognitive impairment. It is believed that natural products can protect the neural cells and system by protecting from damages or promoting regeneration. Therefore, the effects of grape seed extract (GSE) on the hippocampus of aged mice were investigated in this study. twelve old mice were divided into two groups of control and GSE. Animals in the GSE group received 300 mg/kg of GSE for eight weeks via gavage. At the end of treatment, cognition performance was evaluated by Morris water maze (MWM) and passive avoidance tests. Hippocampal neurogenesis, synaptogenesis and DNs production were evaluated with immunohistochemistry and histological evaluations on 5-micron coronal tissue sections. The hippocampal mean number of double cortin positive cells (DCX+) per unit area, as well as synaptophysin expression in the GSE group, were significantly higher than the control group (p < 0.01). The frequency of DNs in the GSE group was lower than the control group (p < 0.05). Behavioral tests showed that GSE improves memory and learning performance. Consuming GSE in the elderly can potentially alleviate the age-related reduction of hippocampal neurogenesis and synaptogenesis. It is also able to decrease hippocampal DNs production and increase memory and learning. [ABSTRACT FROM AUTHOR]

Background: The atrazine is widely used in the world as herbicide. It has been shown that atrazine can transmit from mother to their offspring via the placenta and the breast milk. Recent studies also confirmed that atrazine has ability to damage to the central nervous system. Since hippocampus is an important part of the brain that plays a key role in memory and learning, we evaluated the effects of atrazine exposure during pregnancy and lactation on the hippocampal cells and spatial memory in the male offspring of mice. Materials and methods: Twenty four pregnant Balb/C mice were divided into three groups of atrazine 10 mg/kg, atrazine 50 mg/kg and normal saline (n = 8). Atrazine and normal saline were given by gavage to the animals. Daily treatment with atrazine or normal saline began from gestational day (GD) 6 and continued until postnatal day (PD) 23. At the end of the treatments, brains of the male offspring were collected and histological studies were performed to detect apoptotic cells and dark neurons (DNs) in their hippocampus. Moreover, eight male offspring from each group were weaned and housed until adulthood (PD75). Then, learning and spatial memory were examined using Morris water maze (MWM) and passive avoidance (PA) tests. Results: The histological results of this study showed that apoptotic cells and DNs were significantly high in the offspring hippocampus in atrazine-exposed groups. Furthermore, the results of the behavioral tests indicated that learning and memory of offspring in the atrazine groups were significantly lower than in the normal saline group. Conclusions: Maternal exposure to atrazine during pregnancy and lactation periods increases the apoptotic cells and DNs in the hippocampus of the mice offspring and impairs their learning and spatial memory. [ABSTRACT FROM AUTHOR]