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#29047244   2017/10/19 Save this To Up

Effects of Autologous Platelet-Rich Plasma on Regeneration of Damaged Endometrium in Female Rats.

To investigate whether autologous platelet-rich plasma (PRP) treatment can improve regeneration of the endometrium in an experimental model of ethanol-induced damage.

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#28974974   2017/10/04 Save this To Up

Effects of salbutamol on the inflammatory parameters and angiogenesis in the rat air pouch model of inflammation.

In the present study, effects of salbutamol on the inflammatory parameters, angiogenesis, interleukin-1 beta (IL-1β) and vascular endothelial growth factor (VEGF) levels were investigated in an air pouch model of inflammation. Inflammation was induced by intrapouch administration of 1% solution of sterile carrageenan in male Wistar rats. Salbutamol (125, 250 and 500 µg/rat) and salbutamol (500 µg/rat) plus propranolol (100 μg/rat) were injected intrapouch. After 6 and 72 h, fluid inside the pouches was collected to measure volume of exudates, leukocytes number and IL-1β levels. To determine angiogenesis, the granulation tissues were dissected out and weighed 3 days after carrageenan injection, then hemoglobin concentration was assessed using a hemoglobin assay kit. In addition, amount of VEGF in the exudates was measured 72 h after induction of inflammation. Leukocyte accumulation and the volume of exudates were significantly inhibited by salbutamol administration. In addition, salbutamol decreased the production of VEGF and IL-1β. Moreover, all used doses of salbutamol significantly inhibited angiogenesis. Interestingly, effects of salbutamol on the attenuation of angiogenesis and inflammatory parameters was similar to diclofenac sodium. Co-administration of propranolol with salbutamol clearly reversed anti-inflammatory effects of salbutamol. Salbutamol can decrease acute and chronic inflammation by β2-adrenergic receptors activation. The observed IL-1β and VEGF inhibitory properties of salbutamol may be responsible for anti-inflammatory and anti-angiogenic effect of the agent.

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#28912867   2017/09/15 Save this To Up

Protective effect of controlled release of cytokine response modifier A from chitosan microspheres on rat chondrocytes from interleukin-1β induced inflammation and apoptosis.

The aim of the present study was to investigate the protective effect of cytokine response modifier A (CrmA) released from chitosan (CS) microspheres in a controlled manner on interleukin (IL)-1β-induced inflammation and apoptosis in chondrocytes. The CrmA release kinetics were characterized by an initial burst release, which was reduced to a linear release over 8 days. Furthermore, chondrocytes were isolated from 1-week-old Sprague Dawley rats. The cell culture was established by stimulation with 10 ng/ml IL-1β and subsequent incubation with CS-CrmA microspheres. Following stimulation with IL-1β, the viability of chondrocytes was decreased. However, the cell viability was attenuated by CS-CrmA microspheres as revealed by a cell counting kit-8 assay. CS-CrmA microspheres significantly inhibited IL-1β-induced inflammation in chondrocytes by attenuating increases in the gene expression levels of inducible nitric oxide synthase and cyclooxygenase-2, as well as the concentrations of nitric oxide and prostaglandin E2. CS-CrmA microspheres significantly decreased the number of apoptotic chondrocytes induced by IL-1β as indicated by a terminal deoxyribonucleotide transferase deoxyuridine triphosphate nick-end labeling assay. In addition, CS-CrmA microspheres blocked IL-1β-induced chondrocyte apoptosis by increasing B-cell lymphoma 2 (Bcl-2) and decreasing Bcl-2-associated X protein, caspase-3 and poly adenosine diphosphate-ribose polymerase expression at the mRNA and protein levels, as indicated by reverse-transcription quantitative polymerase chain reaction and western blot analysis, respectively. The results of the present study revealed that CS-CrmA microspheres, as a controlled release system of CrmA, may protect rat chondrocytes from IL-1β-induced inflammation and apoptosis via regulating inflammatory and apoptosis-associated genes.

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#28910961   2017/09/15 Save this To Up

Paeonol alleviates interleukin-1β-induced inflammatory responses in chondrocytes during osteoarthritis.

Interleukin-1β (IL-1β)-induced inflammatory responses in chondrocytes play an important role in the pathogenesis of osteoarthritis (OA). Searching medicines that affect IL-1β-mediated chondrocytes function is critical in developing therapies for OA. Paeonol, as an important component in traditional Chinese medicine, has anti-inflammatory activity and can offer therapy for a multitude of inflammatory-related diseases. The purpose of this study was to investigate whether paeonol could alleviate the progression of OA through inhibition of IL-1β-induced inflammatory responses in chondrocytes. The cell counting kit-8 assay, 5-ethynil-2'-deoxyuridine staining, hoechst 33258 staining and flow cytometric staining were used to observe the chondrocytes proliferation and apoptosis. Western blot and quantitative real-time PCR were applied to examine the expression of extracellular matrix and cartilage degrading enzymes. Reactive oxygen species (ROS) production was monitored by 2',7'-dichlorodihydrofluoresce in diacetate staining. Furthermore, paeonol was intra-articularly injected into joint capsule in destabilized medial meniscus (DMM)-induced OA rat model for 8 and 12 weeks. The results showed that paeonol could negatively affect IL-1β-mediate chondrocyte apoptosis and proliferation. Application of paeonol attenuated the secretion of cartilage extracellular matrix and cartilage degrading enzymes induced by IL-1β in chondrocytes. Increasing of ROS production by IL-1β was obviously alleviated by paeonol. Besides, paeonol alleviated DMM-induced articular cartilage degeneration in vivo. Taken together, we concluded that paeonol might be used as therapeutic agent for treating OA.

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#28901167   2017/09/13 Save this To Up

Effect of Ischemic Postconditioning on Myocardial Function and Infarct Size Following Reperfusion Injury in Diabetic Rats Pretreated With Vildagliptin.

Cardioprotective actions of ischemic postconditioning (IPostC) against ischemia/reperfusion (I/R) injury are abolished in diabetic hearts. This study has investigated the combined effects of IPostC and vildagliptin (Vilda) on myocardial function and infarct size (IS) against I/R injury in diabetic myocardium.

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#28858844   2017/08/31 Save this To Up

Can regular moderate exercise lead to changes in miRNA-146a and its adapter proteins in the kidney of streptozotocin-induced diabetic male rats?

The aim of this study was to assess whether microRNA-146a and its adapter proteins TNF receptor associated factor6 (TRAF6) and interleukin-1 receptor-associated kinase-1 (IRAK1) may be changed in the kidney of streptozotocin-induced diabetic rats, following regular moderate exercise.

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#28852776   2017/08/30 Save this To Up

Malvidin attenuates pain and inflammation in rats with osteoarthritis by suppressing NF-κB signaling pathway.

Malvidin is one of the most widespread anthocyanidins which exhibits significant antioxidant and anti-inflammatory activity. The aim of this paper is to investigate the effects of Malvidin on osteoarthritis (OA).

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#28738537   2017/07/25 Save this To Up

Phosphodiesterase inhibitor ameliorates neuronal injury in spinal cord ischemia/reperfusion injured rat model.

This study investigated the mechanisms responsible for the neuroprotective effect of sildenafil citrate (SFC) on ischemia-reperfusion spinal cord (SC) injuries. Balloon occlusion of the thoracic aorta was used to induce SC ischemia. The animals (n=30) were separated into three groups: sham, SC injury with saline, and SC injury with 5mg/kg i.p. SFC treatment (SFC). The Basso, Beattie, and Bresnahan (BBB) score was determined to assess neurological function at different time intervals after reperfusion. After 48h, histopathology of the SC was assessed by triphenyltetrazolium chloride (TTC) and Nissl staining. Myeloperoxidase (MPO) activity was estimated using an MPO assay kit. Western blot and ELISA assays were performed to estimate interleukin 1 & 10 (IL-1 & IL-10), tumour necrosis factor α (TNF-α), and nuclear factor (NF-kB) levels in SC tissue homogenates. The study results suggest that treatment with SFC significantly increased neurological function compared with the SC group. In addition, SFC treatment reduced MPO activity compared with the SC group, which subsequently inhibited the infiltration of neutrophils into the SC. There was a significant (p<0.01) decrease in the expression of IL-1 and TNF-α, and an increase in the expression of IL-10 in SFC tissue homogenates compared with SC tissues. Moreover, SFC treatment inhibited the activation of NF-kB in the SC after injury. This study shows that SFC exerts a neuroprotective effect on the SC after ischemia/reperfusion injury by attenuating inflammatory mediators.

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#28391163   2017/04/09 Save this To Up

Peroxiredoxin 4 inhibits IL-1β-induced chondrocyte apoptosis via PI3K/AKT signaling.

Chondrocytes apoptosis induced by reactive oxygen species (ROS) plays a critical role in the pathogenesis of osteoarthritis (OA). Peroxiredoxin 4 (PRDX4), a member of the PRDX family, is essential for removing metabolic free radicals and reducing intracellular ROS. In this study, we sought to investigate the roles of PRDX4 on interleukin 1β (IL-1β)-induced chondrocyte apoptosis.

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#28245468   2017/02/28 Save this To Up

Raf Kinase Inhibitor Protein Attenuates Ischemic-Induced Microglia Cell Apoptosis and Activation Through NF-κB Pathway.

Acute ischemic stroke is one of the most important factors leading to disability and death with the characterization of accumulated neuron death and injured supportive neurovascular structures. Raf-1 kinase inhibitory protein (RKIP) is a key molecule in cell response to survival or death stimuli. However, the role of RKIP in stroke is worthy to be further studied.

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