Biomagnetic of Apatite-Coated Cobalt Ferrite: A Core–Shell Particle for Protein Adsorption and pH-Controlled Release

Magnetic nanoparticle composite with a cobalt ferrite (CoFe2O4, (CF)) core and an apatite (Ap) coating was synthesized using a biomineralization process in which a modified simulated body fluid (1.5SBF) solution is the source of the calcium phosphate for the apatite formation. The core–shell structure formed after the citric acid–stabilized cobalt ferrite (CFCA) particles were incubated in the 1.5 SBF solution for 1 week. The mean particle size of CFCA-Ap is about 750 nm. A saturation magnetization of 15.56 emug-1 and a coercivity of 1808.5 Oe were observed for the CFCA-Ap obtained. Bovine serum albumin (BSA) was used as the model protein to study the adsorption and release of the proteins by the CFCA-Ap particles. The protein adsorption by the CFCA-Ap particles followed a more typical Freundlich than Langmuir adsorption isotherm. The BSA release as a function of time became less rapid as the CFCA-Ap particles were immersed in higher pH solution, thus indicating that the BSA release is dependent on the local pH

Osteoporosis in diabetes mellitus: Possible cellular and molecular mechanisms

Osteoporosis, a global age-related health problem in both male and female elderly, insidiously deteriorates the microstructure of bone, particularly at trabecular sites, such as vertebrae, ribs and hips, culminating in fragility fractures, pain and disability. Although osteoporosis is normally associated with senescence and estrogen deficiency, diabetes mellitus (DM), especially type 1 DM, also contributes to and/or aggravates bone loss in osteoporotic patients. This topic highlight article focuses on DM-induced osteoporosis and DM/osteoporosis comorbidity, covering alterations in bone metabolism as well as factors regulating bone growth under diabetic conditions including, insulin, insulin-like growth factor-1 and angiogenesis. Cellular and molecular mechanisms of DM-related bone loss are also discussed. This information provides a foundation for the better understanding of diabetic complications and for development of early screening and prevention of osteoporosis in diabetic patients

Agomelatine, venlafaxine, and running exercise effectively prevent anxiety- and depression-like behaviors and memory impairment in restraint stressed rats.

Several severe stressful situations, e.g., natural disaster, infectious disease out break, and mass casualty, are known to cause anxiety, depression and cognitive impairment, and preventive intervention for these stress complications is worth exploring. We have previously reported that the serotonin-norepinephrine-dopamine reuptake inhibitor, venlafaxine, as well as voluntary wheel running are effective in the treatment of anxiety- and depression-like behaviors in stressed rats. But whether they are able to prevent deleterious consequences of restraint stress in rats, such as anxiety/depression-like behaviors and memory impairment that occur afterward, was not known. Herein, male Wistar rats were pre-treated for 4 weeks with anti-anxiety/anti-depressive drugs, agomelatine and venlafaxine, or voluntary wheel running, followed by 4 weeks of restraint-induced stress. During the stress period, rats received neither drug nor exercise intervention. Our results showed that restraint stress induced mixed anxiety- and depression-like behaviors, and memory impairment as determined by elevated plus-maze, elevated T-maze, open field test (OFT), forced swimming test (FST), and Morris water maze (MWM). Both pharmacological pre-treatments and running successfully prevented the anxiety-like behavior, especially learned fear, in stressed rats. MWM test suggested that agomelatine, venlafaxine, and running could prevent stress-induced memory impairment, but only pharmacological treatments led to better novel object recognition behavior and positive outcome in FST. Moreover, western blot analysis demonstrated that venlafaxine and running exercise upregulated brain-derived neurotrophic factor (BDNF) expression in the hippocampus. In conclusion, agomelatine, venlafaxine as well as voluntary wheel running had beneficial effects, i.e., preventing the restraint stress-induced anxiety/depression-like behaviors and memory impairment

Experimental design and time-dependent changes in the physical and biochemical parameters in restraint stressed rats.

<p>(A) Timeline diagram shows restraint stress induction protocol and behavioral tests. All rats were acclimatized for 1 week prior to 1-, 4-, or 8-week stress induction (black). One- and 4-week groups, were subjected to preceding stress-free period of 7 and 4 weeks (gray), respectively. Behavioral tests, i.e., elevated plus-maze (EPM), elevated T-maze (ETM), novel object recognition (NOR), Morris water maze (MWM), and forced swimming test (FST), were performed at the end of stress session. (B) Baseline body, (C) final body weight, (D) weight gain, (E) daily food intake, (F) dry weight of adrenal gland, and (G) dry adrenal gland weight normalized by body weight (BW) in 1-, 4-, and 8-week restraint stressed rats. (H) Glucocorticoid receptor (GR) protein expression normalized by β-actin in control and 1-week stressed rats. <i>Inset</i>: representative electrophoresis bands of GR and β-actin. (I–J) Serum and urinary corticosterone levels in 4-week stressed rats. Numbers of animals are noted in parentheses. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001 stress vs. control.</p

Expression of brain-derived neurotrophic factor (BDNF) in stressed rats pre-treated with drugs and exercise.

<p>Hippocampal BDNF protein expression normalized by β-actin in 4-week stressed rats subjected to agomelatine (Ago) or venlafaxine (Vlx) treatment or voluntary wheel running (Ex) as determined by Western blot analysis. <i>Inset</i>: representative electrophoresis bands of BDNF and β-actin. Numbers of animals are noted in parentheses. ^†<i>p</i> < 0.05, ^†††<i>p</i> < 0.001 compared with vehicle (Veh)-treated group.</p

Experimental design and the effects of pharmacological treatments and voluntary wheel running on physical and biochemical parameters in stressed rats.

<p>(A) Timeline diagram shows voluntary wheel running and pharmacological treatment protocols. After 1-week acclimatization, rats were divided into one control (vehicle-treated (Veh)/sedentary) and three experimental groups, i.e., agomelatine-treated (Ago), venlafaxine-treated (Vlx), and running (Ex) groups. Drug administration and exercise intervention were given for 4 weeks (pre-treatment), followed by 4-week stress exposure (stress induction), during which rats received neither drug treatment nor exercise intervention. Behavioral tests were performed at the end of stress induction period. (B) Running distance per day in control and stressed groups. Body weight gain and daily food intake, after pre-treatment (C–D, respectively) and after stress induction period (E–F, respectively). (G) Dry adrenal gland weight normalized by BW, (H) dry heart weight, and (I) dry heart weight normalized by body weight (BW) in sedentary and running rats. The control group was stress-free, whereas the stress group was exposed to 4-week restraint stress. (J) Serum corticosterone levels in stressed rats subjected to each treatment. Pre-Ex, pre-exercise period. Numbers of animals are noted in parentheses. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001 exercise group vs. control (Veh/sedentary) group. ^†<i>p</i> < 0.05, ^††<i>p</i> < 0.01, ^†††<i>p</i> < 0.001 each experimental group vs. stressed (Veh/sedentary) group. ^##<i>p</i> < 0.01 stressed sedentary group vs. sedentary control group.</p

Time-dependent changes in the stress-induced anxiety-like behaviors in rats as determined by EPM and ETM.

<p>(A) Percent open arm entry, (B) percent open arm time, (C) percent closed arm entry, (D) percent closed arm time, and (E) total number of entries in 1-, 4-, and 8-week stressed male rats, as determined by elevated plus-maze (EPM). (F) One-way escape latency, (G) baseline time, (H) avoidance 1, and (I) avoidance 2 in stressed rats, as determined by elevated T-maze (ETM). Numbers of animals are noted in parentheses. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001 stress vs. control.</p