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Pterostilbene attenuates myocardial ischemia-reperfusion injury via the phosphatidylinositol 3'-kinase-protein kinase B signaling pathway.

The current study aimed to evaluate the cardioprotective effects of pterostilbene (PTB) on myocardial ischemia-reperfusion (I/R) injury in rats and identify its possible underlying mechanisms of action. A rat I/R model was established by ligating the left anterior descending coronary artery for 30 min and releasing the ligature to induce reperfusion for 120 min. Serum creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) levels were measured using CK-MB and LDH assay kits and myeloperoxidase (MPO) activity in the myocardium was evaluated using an MPO assay kit. Tumor necrosis factor-α, interleukin (IL)-6 and IL-8 levels were assayed using ELISA kits. Cardiomyocyte apoptosis was measured using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Levels of protein kinase B (Akt) and phosphorylated Akt (p-Akt) were measured using western blotting. The results demonstrated that treatment with PTB significantly reduced cardiomyocyte apoptosis, significantly increased Bcl-2 and p-Akt levels and decreased Bax expression in the hearts of rats subjected to I/R injury. However, the protective effects induced by PTB were attenuated by LY294002, which inhibits Akt activation. The results of the current study suggest that PTB treatment may reduce the I/R injury-induced apoptosis of cardiomyocytes, which is mediated by the phosphoinositide 3-kinase/Akt signaling pathway.

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Neuroprotective effect of tanshinone IIA weakens spastic cerebral palsy through inflammation, p38MAPK and VEGF in neonatal rats.

As one of main active ingredients of salvia miltiorrhizae, which is a traditional Chinese medicine, tanshinone IIA is the basis of its pharmacological activities. In the present study, the effect of tanshinone IIA on weakening spastic cerebral palsy (SCP) in neonatal rats was investigated. Radial arm water maze and holding tests were used to measure the alterations of spastic cerebral palsy, inflammation was measured using an ELISA kit, and western blot analysis was used to analyze the protein expression of p‑p38 mitogen‑activated protein kinase (MAPK) and vascular endothelial growth factor (VEGF). The central mechanisms involved in the mediation or modulation of inflammation, p‑p38 MAPK and VEGF were also investigated. Treatment with tanshinone IIA effectively inhibited spastic cerebral palsy, and the activities of interleukin (IL)‑1β, IL‑6, tumor necrosis factor‑α, monocyte chemoattractant protein 1, cyclooxygenase‑2 and prostaglandin E2 in a neonatal rat model of SCP. Tanshinone IIA effectively suppressed the protein expression of inducible nitric oxide synthase (NOS), phosphorylated (p‑) nuclear factor (NF)‑κB, p‑p38MAPK and VEGF, and activated the phosphorylation of inhibitor of NF‑κB and the protein expression of neuronal NOS in the SCP rat model. These results suggested that the neuroprotective effect of tanshinone IIA weakened SCP through inflammation, p38MAPK and VEGF in the neonatal rats.

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The Effect of Curcumin on TNF-α, IL-6 and CRP Expression in a Model of Polycystic Ovary Syndrome as an Inflammation State.

Having low-grade chronic inflammation such as elevated C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) plays a crucial role in polycystic ovary syndrome (PCOS). This study aimed at investigating the therapeutic effects of curcumin on IL-6, CRP and TNF-α and symptoms of polycystic ovary syndrome.

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Vitamin C plus hydrogel facilitates bone marrow stromal cell-mediated endometrium regeneration in rats.

Intrauterine adhesion (IUA) is a common uterine cavity disease which can be caused by mechanical damage that may eventually lead to infertility and pregnancy abnormalities. Since the effect of therapeutic drugs appears disappointing, cell therapy has emerged as an alternative choice for endometrium regeneration. The aim of this study is to investigate whether the combination of hydrogel Pluronic F-127 (PF-127), Vitamin C (Vc), and a bone marrow stromal cell (BMSC) mixture could be a feasible strategy to improve the endometrial regeneration in a mechanical damage model of IUA in rats.

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Human umbilical cord-derived mesenchymal stem cells ameliorate insulin resistance by suppressing NLRP3 inflammasome-mediated inflammation in type 2 diabetes rats.

Insulin resistance is one of the most common and important pathological features of type 2 diabetes (T2D). Recently, insulin resistance is increasingly considered to be associated with systemic chronic inflammation. Elevated levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in blood are predictive indicators of the development of T2D. Mesenchymal stem cell (MSC)-based therapies have been proven to have potential immunomodulation and anti-inflammatory properties through their paracrine effects; however, the mechanism for the anti-inflammatory effect of MSCs in enhancing insulin sensitivity is still uncertain.

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Curcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-phosphoinositide 3-kinase/protein kinase B-nuclear factor-κB signaling pathway in rat thoracic aorta endothelial cells.

Endothelial cell inflammatory injury is likely required for barrier dysfunction under hyperglycemic conditions. Curcumin (CUR) is well known for its anti-inflammatory effect. However, there have been few reports about the anti-inflammatory effect of CUR induced by high glucose in endothelial cells. The aim of the present study was to investigate the inflammatory effect of high glucose and the anti-inflammatory effect of CUR induced by high glucose in rat thoracic aorta endothelial cells (TAECs).

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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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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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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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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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