Inflammatory Factors
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2022 ◽  
Vol 12 (3) ◽  
pp. 581-587
Wenxu Rao ◽  
Kang Yin

This study aims at investigating the mechanism underlying bone marrow mesenchymal stem cells (BMSC) function in glioma. Glioma cells were administered with plasmids loading NF-κB siRNA, microRNA (miRNA)-189 inhibitor, or miR-189 mimics for transfection followed by analysis of miR-189 expression by RT-qPCR, cell apoptosis by flow cytometry, cell proliferation by MTT assay,invasion and migration by Transwell assay, inflammatory factors secretion by ELISA as well as proteins expression by western blot. A mouse model of glioma was established to detect the in vivo effect of BMSCs. miR-189 was lowly expressed in glioma cell lines but enriched in BMSCs. When miR-189 was silenced, cell proliferation, invasion and migration were potentiated and apoptosis was decreased, along with enhancement of N-cadherin, Vimentin, MMP-2 and and MMP-9, and decline in Bax, cleaved casepase-3 and cleaved PARP. Silencing of NF-κB reversed the effect of miR-189 inhibitor on cell progression, accompanied with reduction of inflammatory factors. BMSCs treatment effectively promoted miR-189 expression in glioma and inactivated TNF-α/NF-κB signaling, thereby suppressing tumor growth. In conclusion, miR-189 derived from BMSC inhibits glioma progression through regulation of TNF-α/NF-κB signaling pathway.

2022 ◽  
Vol 12 (4) ◽  
pp. 841-847
Meijiao Du ◽  
Zhengmei Wang ◽  
Geng Su ◽  
Yunxia Zhou ◽  
Chuan Luo

This study aims to analyze the role of mTOR inhibitor on the expression of miR-211 in rat brain tissue and the biological effect of miR-211 in attenuating seizure. Rats were randomly divided into four groups, and the number of seizures and the duration of single seizure were observed within 24 hours after intervention. The level of miR-211 in brain tissue was detected by RT qPCR, the apoptosis of nerve cells was assessed by TUNEL staining, the level of immune cells was detected by flow cytometry, and the level of serum inflammatory factors was determined by ELISA. The number of seizures and the duration of single seizure in the three groups treated by rapamycin within 24 hours were lower than those in the control group, and the symptom relief in group C was the best. After treatment, the expression level of miR-211 in the brain tissue of epileptic rats increased. TUNEL staining showed that neuronal apoptosis was obvious in epileptic rats. The anti apoptotic ability of group C was the most significant, followed by group D and group B. Compared with group A, the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells in brain tissue of group C were decreased, while the levels of IL-2 and IFN-γ were lower in group C than those in control. In group C (n = 5), the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells were elevated, and the levels of immune related cytokines IL-2 and IFN-γ were higher than those of rats without miR-211 inhibition. mTOR inhibitors can improve the local immune microenvironment, reduce the release of inflammatory factors, and finally decrease the frequency and duration of seizures by up regulating the level of miR-211 in rat brain tissue.

2022 ◽  
Vol 12 (5) ◽  
pp. 1015-1021
Gen Lin ◽  
Ruichun Long ◽  
Xiaoqing Yang ◽  
Songsong Mao ◽  
Hongying Li

Objective: The present study aimed to investigate the role of etomidate in intestinal cell ischemia and hypoxia-reperfusion injury and potential mechanisms. Method: In this study, we establish the intestinal epithelial cells ischemia-reperfusion model in vitro. CCK8 was used to detect cell viability and flow cytometry assay was used to detect apoptosis levels of treated OGD/R model cells. ELISA measured the expression level of oxidative stress factors and inflammatory factors. Furthermore, western blot assay was used to detect the expression the apoptosis-related factors and TNFR-associated factors in treated OGD/R model cells. Result: Etomidate does not affect the activity of intestinal epithelial cells, and can protect intestinal epithelial cells to reduce ischemiareperfusion injury, and the expression of inflammatory factors and oxidative stress in cells with mild intestinal epithelial ischemia-reperfusion injury. Etomidate alleviates apoptosis of intestinal epithelial ischemia-reperfusion injury cells. Etomidate inhibits the activation of traf6-mediated NF-κB signal during ischemia-anoxia reperfusion of intestinal epithelial cells. Conclusion: Taken together, our study demonstrated that etomidate attenuates inflammatory response and apoptosis in intestinal epithelial cells during ischemic hypoxia-reperfusion injury and inhibits activation of NF-κB signaling regulated by TRAF6.

2022 ◽  
Vol 38 (3) ◽  
Lilin Gao ◽  
Shaojie Zhang ◽  
Xuewen Wo ◽  
Xiangpeng Shen ◽  
Qiangyuan Tian ◽  

Objectives: To compare the efficacy and safety of intravenous thrombolysis with alteplase and intravenous thrombolysis with urokinase for patients with acute cerebral infarction. Methods: This prospective study included 140 patients with acute cerebral infarction who were admitted to our hospital between June 2018 and June 2019. They were randomly divided into two groups. The control group (70 cases) was treated with urokinase intravenous thrombolysis, and the observation group (70 cases) was given alteplase intravenous thrombolytic therapy. The treatment efficacy and safety of the two groups were compared. Results: The total effective rate of the observation group was 95.7%, and that of the control group was 78.6%, i.e., the total effective rate of the observation group was significantly superior to the that of the control group (P < 0.05). After treatment, the observation group had significantly lower National Institutes of Health Stroke Scale (NIHSS) score and significantly higher mini-mental state examination (MMSE) score than the control group; the difference was statistically significant (P<0.05). After treatment, the levels of inflammatory factors of both groups significantly decreased compared to before treatment, and the decrease in the observation group was larger than that in the control group (P<0.05). The levels of serum homocysteine (Hcy) and monocyte chemoattractant protein-1 (MCP-1) in the observation group were significantly lower than those in the control group after treatment, and the differences were statistically significant (P<0.05). The incidence of hemorrhagic adverse reaction in the observation group was lower than that in the control group (P<0.05). Conclusion: In the treatment of acute cerebral infarction, ccompared with urokinase, alteplase can further relieve cognitive impairment and promote the recovery of nerve function through inhibiting levels of inflammatory factors and levels of serum Hcy and MCP-1. doi: How to cite this:Gao L, Zhang S, Wo X, Shen X, Tian Q, Wang G. Intravenous thrombolysis with alteplase in the treatment of acute cerebral infarction. Pak J Med Sci. 2022;38(3):---------. doi: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Tian Li ◽  
Xiaojun Ji ◽  
Jingfeng Liu ◽  
Xinjie Guo ◽  
Ran Pang ◽  

Introduction: Increased permeability of the renal capillaries is a common consequence of sepsis-associated acute kidney injury. Vascular endothelial (VE)-cadherin is a strictly endothelial-specific adhesion molecule that can control the permeability of the blood vessel wall. Additionally, autophagy plays an important role in maintaining cell stability. Ulinastatin, a urinary trypsin inhibitor, attenuates the systemic inflammatory response and visceral vasopermeability. However, it is uncertain whether ulinastatin can improve renal microcirculation by acting on the endothelial adhesion junction. Methods: We observed the effect of ulinastatin in a septic rat model using contrast-enhanced ultrasonography (CEUS) to evaluate the perfusion of the renal cortex and medulla. Male adult Sprague-Dawley rats were subjected to cecal ligation and puncture and divided into the sham, sepsis, and ulinastatin groups. Ulinastatin (50,000 U/kg) was injected into the tail vein immediately after the operation. The CEUS was performed to evaluate the renal microcirculation perfusion at 3, 6, 12, and 24 hours after the operation. Histological staining was used to evaluate kidney injury scores. Western blot (WB) was used to quantify the expression of VE-cadherin, LC3II, and inflammatory factors [interleukin -1β (IL-1β), interleukin -6 (IL-6), and tumor necrosis factor-α (TNF-α)] in kidney tissue, and enzyme-linked immunosorbent assay (ELISA) detected serum inflammatory factors and kidney function and early kidney injury biomarker levels. Results: Compared with the sham group, ulinastatin reduced the inflammatory response, inhibited autophagy, maintained the expression of VE-cadherin, and meliorated cortical and medullary perfusion. Conclusion: Ulinastatin effectively protects the adhesion junction and helps ameliorate the perfusion of kidney capillaries during sepsis by the inhibition of autophagy and the expression of inflammatory factors.

2022 ◽  
Vol 5 (1) ◽  
pp. 1
Danik M. Martirosyan ◽  
Mohammad Reza Ashoori ◽  
Alireza Rezaeinezhad ◽  
Fahimeh Jahanbakhshi ◽  
Shaghayegh Pezeshki ◽  

Background: Unmanaged type 2 diabetes mellitus has dangerous consequences, such as neuropathy. Oxidative stress and inflammatory factors play an important role in the development of diabetic neuropathy. Diabetics are prone to mild cognitive impairment, which is a neurological disease. The aim of this study was to investigate the effects of quercetin as a functional food and oxidative agents and inflammatory factors of low-level laser.Methods: In this study, 60 elderly volunteers were selected: 30 normal as a control group and 30 with type 2 diabetes mellitus and mild cognitive impairment. The average age was 75 years old. Groups of diabetic patients were examined for changes in glucose levels, oxidants, antioxidants and inflammatory factors before and after treatment with quercetin and low-level laser therapy–green laser diode with a wavelength of 532 nm at 100 mw and compared with the control group. Changes in the levels of biochemical parameters were performed according to the instructions of the relevant kits. Results: The results of the obtained data analysis showed that there was a significant difference (P value < 0.05) in the levels of glucose, hydrogen peroxide, advanced glycation end-products, malondialdehyde, oxidized-low density lipoprotein, paraoxonase, lipoprotein lipase, and inflammatory factors including TNF-α, interleukin-1 alpha and interleukin-1 beta between diabetic samples before and after treatment with quercetin and laser from control subject samples. There was no significant difference (P value > 0.05) in inflammatory factors between quercetin-treated, laser-treated and both quercetin and laser treated groups. The synergistic effect of quercetin and laser between the quercetin and laser treated group and the untreated group on changes in the levels of biochemical parameters was observed significantly only in advanced glycation end-products, malondialdehyde, oxidized-low density lipoprotein, and paraoxonase.Conclusion: The results showed that quercetin, laser, and their synergistic effect can play a role in reducing some oxidant factors.Keywords: Quercetin, Low-level laser, Inflammatory factors, Oxidative factors, Diabetes mellitus

2022 ◽  
Vol 2022 ◽  
pp. 1-6
Tingju Wei ◽  
Jun Li ◽  
Guowei Fu ◽  
Hui Zhao ◽  
Chen Huang ◽  

Objective. To clarify the protective effect of simvastatin on myocardial ischemia reperfusion injury (MIRI) and the underlying mechanism. Materials and Methods. The MIRI model in rats was firstly constructed. Twenty-four male rats were randomly assigned into the sham group, ischemia-reperfusion (I/R) group, and simvastatin group, with 8 rats in each group. Contents of superoxide dismutase (SOD) and malondialdehyde (MDA), as well as serum levels of CK and inflammatory factors, in rats were determined by the enzyme-linked immunosorbent assay (ELISA). Lactate dehydrogenase (LDH) activity in the three groups was examined. Through flow cytometry and Cell Counting Kit-8 (CCK-8) assay, apoptosis and viability in each group were detected, respectively. Relative levels of HMGB1, Kruppel-like factor 2 (KLF2), eNOS, and thrombomodulin (TM) were finally determined. Results. Simvastatin treatment markedly enhanced SOD activity and reduced contents of MDA, LDH, and creatine kinase (CK) in MIRI rats. The increased apoptosis and decreased viability following MIRI were partially reversed by simvastatin treatment. Besides, MIRI resulted in the upregulation of inflammatory factors and chemokines. Their elevations were abolished by simvastatin. In MIRI rats, simvastatin upregulated KLF2 and p-eNOS. Conclusions. Simvastatin protects inflammatory response at post-MIRI through upregulating KLF2, thus improving cardiac function.

2022 ◽  
Mona Dastgheib ◽  
Seyed Vahid Shetab-Boushehri ◽  
Maryam Baeeri ◽  
Mahdi Gholami ◽  
Mohammad Yahya Karimi ◽  

Abstract Diabetic neuropathy (DN) is the most challenging microvascular complication of diabetes and there is no suitable treatment for it, so the development of new agents to relieve DN is urgently needed. Since oxidative stress and inflammation play an essential role in the development of DN, clearance of these factors are good strategies for the treatment of this disease. According to key role of cyclic adenosine monophosphate (cAMP) in the regulation of oxidative stress and inflammatory pathways, it seems that phosphodiesterase inhibitors (PDEIs) can be as novel drug targets for improving DN through enhancement of cAMP level. The aim of this study was to evaluate the effects of rolipram, a selective PDE4 inhibitor, and pentoxifylline, a general PDE inhibitor on experimental model of DN and also to determine the possible mechanisms involved in the effectiveness of these agents. We investigated the effects of rolipram (1mg/kg) and pentoxifylline (100 mg/kg) and also combination of rolipram (0.5 mg/kg) and pentoxifylline (50 mg/kg), orally for five weeks in rats that became diabetic by STZ (55 mg/kg, i.p.). After treatments, motor function was evaluated by open-field test, then rats were anesthetized and dorsal root ganglion (DRG) neurons isolated. Next, oxidative stress biomarkers and inflammatory factors were assessed by biochemical and ELISA methods, and RT-PCR analysis in DRG neurons. Rolipram and/or pentoxifylline treatment significantly attenuated DN – induced motor function deficiency by modulating distance moved and velocity. Rolipram and/or pentoxifylline treatment dramatically increased the cAMP level, as well as suppressed DN – induced oxidative stress which was associated with decrease in LPO and ROS and increase in TAC, total thiol, CAT and SOD in DRG neurons. On the other hand, the level of inflammatory factors (TNF-α, NF-kB and COX2) significantly decreased following rolipram and/or pentoxifylline administration.The maximum effectiveness was with rolipram and/or pentoxifylline combination on mentioned factors.These findings provide novel experimental evidence for further clinical investigations on rolipram and pentoxifylline combination for the treatment of DN.

2022 ◽  
Vol 12 ◽  
Lei Mu ◽  
Limin Jiang ◽  
Juan Chen ◽  
Mei Xiao ◽  
Wei Wang ◽  

Objective: To study the correlation between serum inflammatory factors, oxidative stress factors and frailty, and cognitive frailty in patients with cerebral small vessel disease (CSVD).Methods: A total of 281 patients with CSVD were selected from Tianjin Huanhu Hospital and Inner Mongolia People's Hospital from March 2019 to March 2021. CSVD was diagnosed by MRI. The FRAIL scale was used to evaluate the frailty of patients. Patients with CSVD with frailty and MMSE score &lt;27 were considered to have cognitive frailty. Patients with non-cognitive frailty were included in the control group. The Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) were used to evaluate the cognitive function of patients with CSVD. The serum interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase 3 (MMP-3), superoxide dismutase (SOD), and malondialdehyde (MDA) of patients with CSVD were detected. The correlation between blood inflammatory factors and oxidative stress factors with the frailty and cognitive frailty patients of CSVD were analyzed. Univariate and multivariate logistic regression were used to analyze the correlation between cognitive frailty and CSVD.Results: Among the patients with CSVD selected in this study, female patients and older patients had a higher proportion of frailty (p &lt; 0.001). In the Frail group, MoCA score and MMSE score were significantly lower than in the Pre-Frail and Robust groups, Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) scores were significantly higher than the Pre-Frail and Robust groups, and the differences were statistically significant (p &lt; 0.05). Serum CRP, IL-6, TNF-α, MMP-3, and MDA levels in the Frail group were higher, but SOD levels were lower. The levels of serum CRP, IL-6, TNF-α, MMP-3, and MDA in patients with CSVD in the Cognitive Frailty group were significantly higher than those of the Control group, while the levels of SOD were significantly lower than those of the Control group, and the differences were significant (p &lt; 0.001). The results of univariate and multivariate logistic regression analysis showed that CRP, TNF-α, MMP-3, and MDA levels were associated with cognitive frailty in patients with CSVD (p &lt; 0.05).Conclusion: The increase of serum CRP, TNF-α, MMP-3, and MDA levels are significantly related to the increased risk of frailty and cognitive frailty in patients with CSVD.

2022 ◽  
Vol 12 ◽  
Zhi Zeng ◽  
Liangyu Fei ◽  
Juntao Yang ◽  
Jun Zuo ◽  
Zelin Huang ◽  

Objective: Osteoporosis is caused by the dysregulation of bone homeostasis which is synergistically mediated by osteoclasts and osteoblasts. MiR-27a-3p is a key inhibitor of bone formation. Hence, unearthing the downstream target gene of miR-27a-3p is of great significance to understand the molecular mechanism of osteoporosis.Methods: Bioinformatics analysis was utilized to find the downstream target gene of miR-27a-3p, and dual-luciferase reporter assay was conducted to validate the interplay of miR-27a-3p and GLP1R. Besides, qRT-PCR, Western blot, and enzyme-linked immunosorbent assay (ELISA) were employed to verify the impact of miR-27a-3p on GLP1R expression and the differentiation, autophagy, and inflammatory response of MC3T3-E1 pre-osteoblasts.Results: Dual-luciferase assay validated that miR-27a-3p directly targeted GLP1R. Additionally, posttreatment of MC3T3-E1 cells with miR-27a-3p mimics resulted in a remarkable decrease in expression levels of GLP1R, cell differentiation marker gene, autophagy marker gene, and AMPK. These results indicated that miR-27a-3p targeted GLP1R to inhibit AMPK signal activation and pre-osteoblast differentiation and autophagy, while promoting the release of inflammatory factors.Conclusion: The miR-27a-3p/GLP1R regulatory axis in pre-osteoblasts contributes to understanding the molecular mechanism of osteoporosis.

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