Journal of Basic and Clinical Physiology and Pharmacology最新文献

Objectives: Olive (Olea europaea L.) plays a promising role in pharmaceutical, nutraceutical, and cosmetic production. On the other hand, olive leaf is widely used in folk medicine due to its antihyperglycemic activity. For this aim, possible effects of olive leaf extract (OLE) in the brain tissue of streptozotocin-induced diabetic rats were investigated.

Methods: A total of 28 male rats were divided into four equal groups as control, diabetic (single dose of 45 mg/kg streptozotocin, i.p.), OLE (500 mg/kg/day), and diabetic + OLE groups. The study was terminated 21 days after the diabetes model was formed. At the end of the study, all the animals were sacrificed and blood and brain tissues were isolated. Relative brain weights, complete blood count, blood glycated hemoglobin, serum glucose, total protein, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, insulin, gonadal hormone levels, production and messenger ribonucleic acid (mRNA) levels of proinflammatory cytokines and mediators, total thiol, total oxidative stress, and total antioxidant status levels and fatty acid composition in brain tissue were measured in all study groups.

Results: In diabetic rats, relative brain weight and serum insulin level decreased, glycated hemoglobin, oxidative stress, production and mRNA level of proinflammatory cytokines and mediators increased, hyperglycemia, hypercholesterolemia and hypertriglyceridemia, degraded fatty acid composition, anemia, leukopenia, and thrombocytopenia occurred. After OLE treatment, a remarkable improvement in most of these parameters, except gonadal hormones, has been observed in diabetic rats.

Conclusions: This study suggests that olive leaf can be a precious neuroprotective agent in diabetes.

Objectives: Seizures are abnormal discharge of neurons in the brain. Ferulic acid (FA) is a phenolic compound with antioxidant and neuroprotective effects. The present study aimed to investigate the role of the nitrergic system in the anticonvulsant effect of FA in pentylenetetrazol (PTZ)-induced seizures in male mice.

Methods: 64 male Naval Medical Research Institute (NMRI) mice weighing 25-29 g were randomly divided into eight experimental groups (n=8). FA at doses 5, 10, and 40 mg/kg alone and in combination with L-nitro-arginine methyl ester (L-NAME) (nitric oxide synthase inhibitor) or L-arginine (L-arg) (nitric oxide [NO] precursor) was administrated (intraperitoneal). PTZ was injected (i.v. route) 30 min after drugs administration (1 mL/min). Seizure onset time was recorded and the nitrite levels of prefrontal cortex and serum were determined by the Griess method.

Results: FA at doses of 10 and 40 mg/kg significantly increased the seizure threshold as well as reduced the serum and brain NO levels in comparison to the saline-received group. Co-administration of the effective dose of FA (10 mg/kg) plus L-arg significantly decreased the seizure threshold in comparison to the effective dose of FA alone. Co-injection of the sub-effective dose of FA (5 mg/kg) with L-NAME significantly increased the seizure threshold as well as significantly decreased the brain NO level in comparison to the sub-effective dose of FA alone.

Conclusions: We showed that the nitrergic system, partially at least, mediated the anticonvulsant effect of FA in PTZ-induced seizures in mice. We concluded that L-NAME potentiated while L-arg attenuated the anticonvulsant effect of FA.

Sarcoma is defined as a tumor located in the thoracic cavity. However, sarcoma can occur on every side of the body. Synovial sarcoma is a rare soft tissue tumor originating from pluripotent with a high malignancy rate. The most common predilection of synovial sarcoma is in the joints. Primary synovial sarcoma of the lung and mediastinum are rare tumors and generally malignant. There are only a few cases have been reported. Definite diagnosis is made by histopathological, immunohistochemistry, and cytogenetic examination. The management strategy for synovial sarcoma requires multimodality treatment with surgery, chemotherapy, and radiotherapy. However, effective and relatively non-toxic therapy for primary synovial sarcoma is still developed. The five years life expectancy is higher if the patient received adjuvant radiotherapy and/or chemotherapy after surgery.

Objectives: Endurance exercise is an effective strategy for maintaining an anti-inflammatory environment and weight management. However, the effect of this type of exercise on decreasing body fat and TNF-α levels and increasing adiponectin levels is controversial. The aims of this study was to prove the effects of weight-bearing vs. non-weight-bearing endurance exercise on reducing body fat and inflammatory markers in obese females.

Methods: 24 obese adolescents were recruited from female students from the State University of Malang. The interventions given in this study were weight-bearing endurance exercise (WBEE), and non-weight-bearing endurance exercise (NWBEE). Serum TNF-α levels and serum adiponectin levels were evaluated using enzyme-linked immunosorbent assay (ELISA). Statistical analysis techniques use paired sample T-test with a significant level of 5%.

Results: Results of the statistical analysis show that the average body fat (PBF, FM, FFM) and TNF-α levels before endurance exercise vs. after endurance exercise in both types of exercise experienced a significant decrease (p≤0.05), while average adiponectin levels in both types of exercise experienced a significant increase before endurance exercise vs. after endurance exercise (p≤0.001).

Conclusions: In general, it can be concluded that weight-bearing and non-weight-bearing endurance exercise with moderate-intensity for 40 min/exercise session reduce body fat and TNF-α levels and increase adiponectin levels as a marker of inflammation in obese female.

Diabetic wounds are of profound clinical importance. Despite immense efforts directed towards its management, it results in the development of amputations, following a diagnosis of diabetic foot. With a better understanding of the complexities of the microbalance involved in the healing process, researchers have developed advanced methods for the management of wounds as well as diagnostic tools (especially, for wound infections) to be delivered to clinics sooner. In this review, we address the newer developments that hope to drive the transition from bench to bedside in the coming decade.

Objectives: Primary Osteoarthritis (OA) is a disease of progressive joints degeneration due to idiopathic causes. Recent evidence showed a positive relationship between OA and metabolic syndrome. This pilot study aimed to assess the baseline level of pro and anti-inflammatory cytokines in OA patients with or without Diabetic Mellitus (DM) and assess the effect of hydrogen peroxide (H₂O₂) in cytokine production.

Methods: Patients with primary hip and knee OA were recruited, and 3 mL of bone marrow was harvested during joint replacement surgery. Bone marrow stromal cells (BMSC) was isolated and cultured in a culture flask for three passages. Later experiment was then sub-cultured in a well plate labeled as the control group and H₂O₂ (0.1 mM) treated group. ProcartaPlex^® Multiplex Immunoassay was performed to measure cytokine levels produced by the BMSC at 0 h, as well as 72 h.

Results: Cytokines such as tumor necrosis factor-alpha, interleukin (IL)-6, IL-8, and IL-1β generally exhibited higher cytokine levels in subjects with DM than in nonDM subjects at 0 and 72 h. For IL-17, its expression was similar in nonDM and DM groups at 0 and 72 h. Cytokine IL-10 showed no significant difference in both the groups while DM and nonDM groups treated with H₂O₂ showed decreased IL-4 levels compared to control groups at 72 h. Bone marrow cells from DM-OA are more vulnerable to chemical insult and are associated with higher levels of proinflammatory cytokines production and lower IL-4 level production.

Conclusions: This study provides a clue that management of OA with co-morbidity like DM needs future studies.

Background: Diabetic cardiometabolic disorders are characterized by significant changes in cardiac metabolism and are increased in postmenopausal women, which emphasize the role of 17β-estradiol (E2). Despite this, there are few safe and effective pharmacological treatments for these disorders. The role of G protein-coupled estrogen receptor (GPR30), which mediates the non-genomic effects of E2, is mostly unexplored.

Methods: In this study, we used ovariectomy (menopausal model) and type 2 diabetic (T2D) rats' models to evaluate the preclinical action of G-1 (GPR30 agonist) against cardiometabolic disorders. T2D was induced by a high-fat diet and a low dose of streptozotocin. G-1 was administrated for six weeks after the establishment of T2D.

Results: We found that G-1 counteracts the effects of T2D and ovariectomy by increasing the body weight, reducing fasting blood sugar, heart weight, and heart weight to body weight ratio. Also, both ovariectomy and T2D led to decreases in the cardiac protein levels of hexokinase 2 (HK2) and GLUT4, while G-1-treated female rats reversed these changes and only increased HK2 protein level. In addition, T2D and ovariectomy increased glucose and glycogen content in the heart, but G-1 treatment significantly reduced them.

Conclusions: In conclusion, our work demonstrates that G-1 as a selective GPR30 agonist is a viable therapeutic approach against T2D and cardiometabolic diseases in multiple preclinical female models.

Objectives: Regular treadmill exercise may result in changes in pro-inflammatory cytokines and oxidative stress. However, the way acute treadmill exercise mechanisms affect the changes in pro-inflammatory cytokines and oxidative stress in obese has not been comprehensively exposed. This study aimed to analyze the pro-inflammatory cytokines and oxidative stress between 30 min before treadmill exercise and 24 h after treadmill exercise in obese adolescents.

Methods: A total of 20 obese females aged 19-24 years were recruited from female students and given one session of treadmill exercise with an intensity of 60-70% HR_max. Thiobarbituric acid reactive substance (TBARS) was used to analyze serum levels of MDA, while enzyme-linked immunosorbent assay (ELISA) was used to analyze serum levels of TNF-α and IL-6. Moreover, the independent samples t-test with a significance level of 5% was employed to have the statistical analysis.

Results: The results on 24 h after treadmill exercise and delta (Δ) between CTRL and TREG showed a significant difference (p<0.001).

Conclusions: This study found a decrease in pro-inflammatory cytokines and oxidative stress 24 h after treadmill exercise in obese adolescents. Therefore, treadmill exercise can be a promising strategy for preventing adolescents from obesity as well as preventing disease risks associated with oxidative stress and chronic inflammation.

Brain-derived neurotrophic factor (BDNF) is a crucial neurotrophic factor adding to neurons' development and endurance. The amount of BDNF present in the brain determines susceptibility to various neurodegenerative diseases. In Alzheimer's disease (AD), often it is seen that low levels of BDNF are present, which primarily contributes to cognition deficit by regulating long-term potentiation (LTP) and synaptic plasticity. Molecular mechanisms underlying the synthesis, storage and release of BDNF are widely studied. New molecules are found, which contribute to the signal transduction pathway. Two important receptors of BDNF are TrkB and p75NTR. When BDNF binds to the TrkB receptor, it activates three main signalling pathways-phospholipase C, MAPK/ERK, PI3/AKT. BDNF holds an imperative part in LTP and dendritic development, which are essential for memory formation. BDNF supports synaptic integrity by influencing LTP and LTD. This action is conducted by modulating the glutamate receptors; AMPA and NMDA. This review paper discusses the aforesaid points along with inducers of BDNF. Drugs and herbals promote neuroprotection by increasing the hippocampus' BDNF level in various disease-induced animal models for neurodegeneration. Advancement in finding pertinent molecules contributing to the BDNF signalling pathway has been discussed, along with the areas that require further research and study.