The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to coronavirus disease 2019 (COVID-19) pandemic. While the common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. The involvement of different organs in severe patients results in lengthening the hospitalization duration and increasing the mortality rate. In this review, we aimed to investigate the involvement of different organs in COVID-19 patients, particularly in severe cases. Also, we tried to define the potential underlying mechanisms of SARS-CoV2 induced multiorgan failure. The multi-organ dysfunction is characterized by acute lung failure, acute liver failure, acute kidney injury, cardiovascular disease, and as well as a wide spectrum of hematological abnormalities and neurological disorders. The most important mechanisms are related to the direct and indirect pathogenic features of SARS-CoV2. Although the presence of angiotensin-converting enzyme 2, a receptor of SARS-CoV2 in the lung, heart, kidney, testis, liver, lymphocytes, and nervous system was confirmed, there are controversial findings to about the observation of SARS-CoV2 RNA in these organs. Moreover, the organ failure may be induced by the cytokine storm, a result of increased levels of inflammatory mediators, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs. Therefore, further investigations are needed to detect the exact mechanisms of pathogenesis. Since the involvement of several organs in COVID-19 patients is important for clinicians, increasing their knowledge may help to improve the outcomes and decrease the rate of mortality and morbidity.

Objectives: The purpose of this study is investigating curcumin role in mood alterations in male rats after spinal cord injury through focusing on the involvement of NLRP3 inflammasome. Methods: Fourteen  adualt male Wistar rats (220–250 g) were divided to five animal groups (n = 8 per group): Control: healthy animals which  received normal saline for 14 days; spinal cord injury: spinal cord injury-induced animals which received normal saline for 14 days; spinal cord injury + curcumin (20, 40, and 80 mg/kg/ i.p): spinal cord injury-induced animals treated with 3 doses of curcumin for 14 days. To assess the mood of animals, the elevated plus maze test, forced swimming test, tail suspension test, and open field test were performed. Graph-pad prism software was used for data analysis. Statistical analysis was done by one-way ANOVA with Tukey’s post hoc test. P < 0.05 was statistically significant. Results: Treatment with curcumin with two doses of 40 and 80 mg/kg increased open arm time and decreased close arm time as compared to the spinal cord injury group. The administration of curcumin (40 mg/kg and 80 mg/kg) enhanced the altered behaviors. Spinal cord injury caused an increase in the protein levels NLRP3, ASC and Casp1 in the hippocampus of animals as compared to the sham group. Curcumin regulated the protein levels of NLRP3, ASC and Casp1 in the hippocampus of animals. Conclusion: Depression is prevalent in person with spinal cord injury and our findings indicated that curcumin appears to constitute a suitable agent to reduce neuroinflammation and through it, relieve a depressive-like state.

Background The antidiabetic and antioxidant effects of Trigonella foenum-graceum have been suggested. The effects of hydroalcoholic extract of the plant seeds and metformin against the diabetes-induced memory impairment were investigated. Materials and methods The rats were treated: (1) control, (2) diabetic (3–6) and diabetic rats treated by 50, 100 and 200 mg/kg of the plant extract or metformin. The rats were diabetic by streptozotocin (STZ, 55 mg/kg). After the passive avoidance test, malondialdehyde (MDA), nitric oxide (NO) metabolites, total thiol (SH), catalase (CAT) and superoxide dismutase (SOD) were determined in the brain. Results In the diabetic group, at 3, 24 and 48 h after receiving a shock, the latency to enter the dark room was lower than for the controls (p < 0.001). All doses of the extract and metformin increased the latencies to enter the dark at 3 and 24 h after the shock treatment (p < 0.05–p < 0.001). Additionally, the two higher doses of the extract and metformin increased the latency at 48 h after the shock (p < 0.05–p < 0.001). Diabetes also elevated MDA and NO metabolites, while it reduced thiol, SOD and CAT in the hippocampal and cortical tissues (p < 0.001). Treatment of the diabetic animals by the highest dose of the extract and also metformin reduced the MDA and NO metabolites, while it improved thiols, SOD and CAT (p < 0.01–p < 0.001). Conclusions Based on our findings, metformin and the hydro-alcoholic extract from the T. foenum-graceum seed prevented memory deficits resulting from diabetes. Preventing oxidative damage in the brain may at least, in part, be responsible for the positive effects of the extract and metformin.

Diabetes mellitus is a metabolic disorder with increasing global prevalence. It is characterized by impaired glucose utilization that leads to chronic hyperglycemia which is a result of the body's inability to produce insulin (diabetes type I) or inability to make use of insulin (diabetes type II). Long-term hyperglycemia can cause damage to multiple systems, and microvascular and macrovascular complications lead to myocardial infarction, blindness, stroke and renal failure. Diabetes affected 382 million people globally in 2013, and it is estimated to rise up to 592 million by 2035. In spite of its management, both microvascular and macrovascular complications partly linked to oxidative stress are not efficiently prevented. Glibenclamide was approved on the U. S. market for treatment of diabetes type II in 1984. ATP-sensitive potassium channels (KATP) are widely distributed and present in a number of tissues including muscle, pancreatic beta cells and the brain. Glibenclamide closed KATP channels, which leads to depolarization of the cells and insulin secretion. Acupuncture is also a very significant therapeutic method in the complementary medicine. ST36 (Zusanli), CV4 (Guanyuan) and CV12 (Zhongwan) are several acupoints that have been used for treatment of diabetes. In this study for evaluating the effects of glibenclamide and electroacupuncture, 3 parameters such as malondialdehyde, ferric reducing antioxidant power and thiol will be measured. Malondialdehyde (MDA) is the organic compound and it is a marker for oxidative stress. Antioxidants are compounds that inhibit oxidation. Oxidation is a chemical reaction that can produce free radicals, thereby leading to chain reactions that may damage the cells of organisms. Antioxidants such as FRAP and thiol are useful parameters of assessment of oxidative stress. The aim of this study was to evaluate the effects of Electroacupuncture (EA) plus glibenclamide (G) as a novel therapy on diabetic rats and maybe for human. Fifty-four male Wistar rats were randomly divided to 9 groups: 1 non-diabetic control group and 8 diabetic groups (1 sham control group and 7 experimental groups; D/G 2.5 mg/kg, D/G 5 mg/kg, D/G 10 mg/kg, EA, D/EA/G 2.5 mg/kg, D/EA/G 5 mg/kg, and D/EA/G 10 mg/kg). Diabetes was induced by intraperitoneal injection of streptozotocin with high-fat diet. At the end of course, blood samples were obtained. Combination therapy of EA and glibenclamide 5 mg/kg decreased blood glucose better than single therapies (p<0.05) and showed 41 percent decrease in blood glucose as compared to D/G 5 mg/kg group. Combination of EA and glibenclamide 10 mg/kg showed the best effect for decreasing the malondialdehyde level (p<0.05) and also showed 43 percent decrease in comparison to D/G 10 mg/kg group. Combination of glibenclamide 2.5 mg/kg and EA increased the FRAP level better than other treatment groups (P<0.001) andachieved the ferric reducing antioxidant power level near to normal range. Combination of glibenclamide 10 mg/kg with EA increased the thiol concentration better than other treatment groups (P<0.001) and showed 4 percent increase in thiol concentration as compared to D/G 10 mg/kg group. These findings suggest that EA potentiates the effect of glibenclamide to protect animal model and maybe human against oxidative stress and damage.

Sarcoidosis is a multi-system disorder of granulomatous inflammation which most commonly affects the lungs. Its etiology and pathogenesis are not well defined in part due to the lack of reliable modeling. Here, we present the development of an in vitro three-dimensional lung-on-chip biochip designed to mimic granuloma formation. A lung on chip fluidic macrodevice was developed and added to our previously developed a lung-on-membrane model (LOMM). Granulomas were cultured from blood samples of patients with sarcoidosis and then inserted in the air-lung-interface of the microchip to create a three-dimensional biochip pulmonary sarcoidosis model (3D BSGM). Cytokines were measured after 48 hours. ELISA testing was performed to measure cytokine response difference between LOMM with 3D BSGM. There were statistically significant differences in IL-1ß (P = 0.001953), IL-6 (P = 0.001953), GM-CSF (P = 0.001953), and INF-γ expressions (P = 0.09375) between two groups. The current model represents the first 3D biochip sarcoidosis model created by adding a microfluidics system to a dual-chambered lung on membrane model and introducing developed sarcoid-granuloma to its air-lung-interface.