Introduction. Renin-angiotensin system has a role in inflammation and also is involved in many brain functions such as learning, memory, and emotion. Neuroimmune factors have been proposed as the contributors to the pathogenesis of memory impairments. In the present study, the effect of captopril on spatial memory and synaptic plasticity impairments induced by lipopolysaccharide (LPS) was investigated. Methods. The rats were divided and treated into control (saline), LPS (1 mg/kg), LPS-captopril (LPS-Capto; 50 mg/kg captopril before LPS), and captopril groups (50 mg/kg) before saline. Morris water maze was done. Long-term potentiation (LTP) from CA1 area of hippocampus was assessed by 100 Hz stimulation in the ipsilateral Schaffer collateral pathway. Results. In the LPS group, the spent time and traveled path to reach the platform were longer than those in the control, while, in the LPS-Capto group, they were shorter than those in the LPS group. Moreover, the slope and amplitude of field excitatory postsynaptic potential (fEPSP) decreased in the LPS group, as compared to the control group, whereas, in the LPS-Capto group, they increased compared to the LPS group. Conclusion. The results of the present study showed that captopril improved the LPS-induced memory and LTP impairments induced by LPS in rats. Further investigations are required in order to better understand the exact responsible mechanism(s).

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Background:Renin-angiotensin (Ang)-aldosterone system not only plays a key role in the regulation of circulatory homeostasis, but also it acts as a powerful pro-inflammatory mediator. The aim of this study was to evaluate the effect of captopril (Cap), a known Ang-converting enzyme inhibitor, on inflammation-induced cardiac fibrosis, and heart oxidative stress status in lipopolysaccharide (LPS)-induced inflammation in male rats.Methods:Fifty male rats were randomly divided into five groups control, LPS (1 mg/kg/day), LPS + Cap 10 mg/kg, LPS + Cap 50 mg/kg and LPS + Cap 100 mg/kg. After 2 weeks, blood samples were taken, and hearts were harvested for evaluation of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide metabolite in serum and tissue hemogenate, histopathology (hematoxylin and eosin and Masson's trichrome) and oxidative stress status.Results:Serum IL-6 and TNF-α concentration were higher in LPS group compared to control and Cap reduced them, significantly. Heart TNF-α and IL-6 contents in LPS group were significantly higher than control (P < 0.05). The administration of Cap significantly decreased inflammatory markers level to control (P < 0.05). The higher levels of malondialdehyde and lower antioxidative markers (total thiol, superoxide dismutase, and catalase) in the heart were observed in LPS group and treatment by Cap improved them, dose-dependently. Histopathological study revealed cardiac fibrosis and more collagen content in LPS group which significantly improved by Cap treatment.Conclusions:Treatment by Cap reduced cardiac fibrosis possibly through improving oxidative stress status, and it can be considered to increase cardiac compliance in this condition.

In this study, the effects of Nigella Sativa (NS) hydro-alcoholic extract on lipopolysaccharide (LPS)-induced learning and memory impairments, hippocampal cytokine levels, and brain tissues oxidative damage were investigated in rats. The rats were grouped and treated: (1) control (saline), (2) LPS (1 mg/kg i.p.), and (3-5) 100, 200, or 400 mg/kg NS hydro-alcoholic extract 30 min before LPS injection. The treatment was started since 6 days before the behavioral experiments and continued during the behavioral tests (LPS injection 2 h before each behavioral experiment). Finally, the brains were removed for biochemical assessments. In Morris water maze (MWM) test, LPS increased the escape latency and traveled path compared to control group, whereas all doses of NS hydro-alcoholic extract decreased them compared to LPS group. In passive avoidance (PA) test, the latency to enter the dark compartment in LPS group was shorter than control group while in all treated groups it was longer than LPS group. LPS increased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), and nitric oxide (NO) metabolites, and decreased thiol content, superoxide dismutase (SOD), and catalase (CAT) in the hippocampal tissues compared to control group while NS hydro-alcoholic extract decreased MDA and NO metabolites and increased thiol content, SOD, and CAT compared to LPS group. Findings of the current study indicated that the hydro-alcoholic extract of NS improved the LPS-induced learning and memory impairments induced by LPS in rats by improving hippocampal cytokine levels and brain tissues oxidative damage.

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