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The hippocampus produces growth hormone (GH) and contains GH receptors, suggesting a potential role for GH signaling in the regulation of hippocampal function. In agreement with this possibility, previous investigations have found altered hippocampal function and hippocampal-dependent learning and memory after chronic GH administration or deficiency. In this study we applied GH to in vitro rat hippocampal brain slices, to determine whether GH has short-term effects on hippocampal function in addition to previously documented chronic effects. We found that GH enhanced both AMPA- and NMDA-receptor-mediated excitatory postsynaptic potentials (EPSPs) in hippocampal area CA1, but did not alter GABA(A)-receptor-mediated inhibitory synaptic transmission. GH enhancement of excitatory synaptic transmission was gradual, requiring 60-70 min to reach maximum, and occurred without any change in paired-pulse facilitation, suggesting a possible postsynaptic site of action. In CA1 pyramidal neurons, GH enhancement of EPSPs was correlated with significant hyperpolarization and decreased input resistance. GH enhancement of EPSPs required Janus kinase 2 (JAK2), phosphatidylinositol-3 (PI3) kinase, mitogen-activated protein (MAP) kinase kinase (MEK), and synthesis of new proteins. Although PI3 kinase and MEK were required for initiation of GH effects on excitatory synaptic transmission, they were not required for maintained enhancement of EPSPs. GH treatment and tetanus-induced long-term potentiation were mutually occluding, suggesting a common mechanism or mechanisms in both forms of synaptic enhancement. Our results demonstrate that GH has powerful short-term effects on hippocampal function, and extend the timescale for potential roles of GH in regulating hippocampal function and hippocampal-dependent behaviors.

Abstract:Objectives. Osteoarthritis (OA) Methods. Eighteen male rats divided into three groups; (Lev) group treated with levofloxacin (Lev), (US) group treated with Lev plus US and (LLLT) group treated with Lev plus low level laser therapy. All animals received total of 200 mg injection of Lev. Total of ten sessions of US and laser applied. Results. We found significant decrease of serum IL-1beta, Mankin's score and increase in knee extension angle in both US and LLLT groups compared to Lev group. US significantly lower IL-6, INF-gamma, CRP and significantly elevate IL-10 in US group compared to Lev and LLLT groups.Conclusion. Based on our finding, US may provide better therapeutic effect compared to LLLT in knee osteoarthritis as indicated by reduction of inflammatory cytokines, elevation of anti-inflammatory cytokines and better histopathological score.

Abstract:Objective: Vitamin Methods: Animals were divided into four groups; (C) saline-treated, (VC) vitamin C-treated, (NIC) nicotinetreated, all were for 3 weeks, and (NIC+VC) is given vitamin C for 3 days prior, with nicotine injection and 2 days thereafter. Results: Present work showed that nicotine exposure caused significant reduction in total body weight, relative liver and kidney weights, elevated malondialdehyde (MDA), alanine transaminase (ALT), aspirate transaminase (AST), and alkaline phosphatase (ALP) in both hepatic and renal tissues. Co-exposure to nicotine and vitamin C maintained normal liver and kidney weight, significantly lowered MDA, ALT, AST, ALP and elevated glutathione in both hepatic and renal tissues compared NIC group as well as controls. Nicotine administration resulted in shedding, necrosis, and loss of brush border of cells covering proximal and distal convoluted tubules of kidney. The liver in the nicotine-treated group showed vacuolated cytoplasm of hepatocytes, with dilated central vein and sinusoids and mitochondrial destruction. Immunohistochemistry showed dense PCNA immunostaining in the livers of nicotine-treated rats. Vitamin C induced partial correction of nicotine-induced histopathological damage of liver and kidney and significant elevation in PCNA expression. Conclusion:The results of present work suggested that vitamin C has a promising prophylactic effect against nicotine-induced oxidative damage of liver and kidney.

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Objectives to investigate the possible mechanism underlying the protective effect of growth hormone (GH) on hippocampal function during periods of acute stress. Methods the effects of coapplication of GH and corticosterone (CORT) at different concentration on field excitatory postsynaptic potential (fFEPSPs) of hippocampal slices of rats at two different age groups were examined. Also, the protein expression of N-methyl-D-aspartate receptor (NMDARs) subunits; NR1, NR2B, and NR2A in hippocampal brain slices treated with artificial cerebrospinal fluid (ACSF) or low concentration of CORT alone or both CORT and GH for three hours were measured. Results We found an additive effect of co-application of CORT and GH on hippocampal synaptic transmission compared to CORT alone. Furthermore, we found that the combined use of low concentration of GH and CORT have significantly higher effects on enhancement of fFEPSPs in old rats compared to young ones. We showed that both GH and CORT enhanced protein expression of NR2A subunit of NMDARs. Meanwhile, we demonstrated that the coexposure to low concentration of GH and CORT significantly enhanced NR2B expression and increased the NR2B/NR2A. In contrast, perfusion with CORT alone caused significant suppression in NR1 and NR2B protein expression and decrease in NR2B/NR2A. Conclusion we suggest that NMDARs provide potential target for mediating GH potential protective effect against stress and age related memory and cognitive impairment.

Metabolic side effects of atypical antipsychotics are an important cause of deterioration of cognitive function and failure of drug adherence. The antifatty effect trypsin/chymotrypsin (T/C) and their mechanisms of action remain unclear. To investigate possible therapeutic effect of T/C in rat model of chronic olanzapine (OLZ) – induced hepatic steatosis. Twenty rats were divided into two groups: control (C), given distilled water, and O, given 1 mg/kg of OLZ orally daily for 7 weeks. Then, both groups were given T/C 3 enzyme activity unit (EAU)/kg orally as an add-on treatment daily for the next 5 weeks and were named T/C or T/C+O groups. Rat performance in radial arm water maze was tested twice before and after T/C treatment. We measured liver enzymes, alpha-1 antitrypsin, albumin, total protein, direct and total bilirubin, inflammatory cytokines, and lipoprotein serum levels. Liver samples were collected for histopathology and Ki67 expression. The T/C add-on caused significant reduction in OLZ-induced elevation of alanine transaminase (ALT; P < 0.01), aspartate transaminase (AST; P < 0.001), alkaline phosphatase (ALP; P < 0.05), total cholesterol (Tc; P < 0.01), low-density lipoproteins (LDL-c; P < 0.05), steatosis score (P < 0.001), hepatocyte necrosis (P < 0.01), and significantly increased Ki67 expression (P < 0.01). The T/C add-on to OLZ provided protection against hepatic steatosis, elevated enzymes, and disturbed lipid profile and increased Ki67 without disturbing memory function.

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