Effect of MEK6 Gene and Salt Treatment on Adipogenesis in MEK6 Over-expressed 3T3-L1 Cells (P21-070-19)

Abstract Objectives Both obesity and obesogenic environments(OE) to induce the fat accumulation are being the risk factors of various metabolic diseases. By 6 year-cohort study, we found that MEK6 gene and salt intake were positively related with inducing obese as part of OE factors such as lifestyle, genes, and eating habits etc. Objectives of study are to find the effects of MEK6 gene and salt treatment on adipogenesis using MEK6 over-expressed 3T3-L1 cells. Methods After transformation for MEK6 over-expressed 3T3-L1 with lipofectamine 3000 (Invitrogen, California, USA) was confirmed by PCR method, salt was treated as 50 mM in the form of NaCl without cytotoxicity (MTT assay). Cell differentiation and TG synthesis (Oil Red O; ORO & DAPI/Nile red staining), and protein expression (western blotting analysis) associated with adipogenesis genes (PPAR-γ, C/EBP-α & aP2) and adipocytokines (adiponectin & leptin) were performed. ELISA kits were used for estimating inflammatory factors such as TNF-α, IL-1β, IL-10, MCP-1, PAI-1 etc. Real-time oxygen consumption in alive cells was measured every 17 seconds for 100 minutes. (Mito-Xpress O2 consumption array kit) All analyses were performed using SAS9.1 software and p-values of <0.05 were interpreted as statistically significant. Results We confirmed the salt induced the protein expression associated with adipogenesis (PPAR-γ, C/EBP-α and aP2) in both control and MEK6 over-expressed cells. The levels of inflammatory cytokine factors (TNF-α, IL-1β, IL-10) were also increased by salt treatment in both groups. We found that obesity-linked metabolism such as lipolysis, insulin resistance, and adipocyte production were significantly higher in MEK6 over-expressed cells than them in the control. However, the leptin level did not seem to be associated with MEK6 gene. Salt also increased O2 consumption in both groups but the time to reach maximum of O2 consumption in MEK6 over-expressed cells was slower than the case of control. MEK6 might be associated with mitochondria function to control O2 consumption. Conclusions The obesity metabolism related adiopgenesis in 3T3-L1 was activated by MEK6 expression and salt treatment. These findings will contribute to a future study for finding MEK6 linked mechanisms involved in adipogenesis and for setting DRI of salt intake in obese Koreans. Funding Sources This work was funded by the Ministry of Health&Welfare, Republic of Korea grant number: HI17C0863.

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LIPUS inhibits inflammation and catabolism through the NF‐κB pathway in human degenerative nucleus pulposus cells

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02739-1 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Weiwei Yi ◽

Qing Chen ◽

Chuan Liu ◽

Kaiting Li ◽

Bailong Tao ◽

...

Keyword(s):

Protein Expression ◽

Real Time ◽

Signaling Pathway ◽

Nucleus Pulposus ◽

Real Time Pcr ◽

Inflammatory Factors ◽

Nucleus Pulposus Cells ◽

Tnf Α ◽

Gene And Protein Expression ◽

Collagen Ii

Abstract Background Low-intensity pulsed ultrasound (LIPUS) is a safe and noninvasive rehabilitative physical therapy with anti-inflammatory effects. The current study investigated the effect of LIPUS on the inflammation of nucleus pulposus (NP) cells and its underlying mechanism. Methods Human NP cells were acquired from lumbar disc herniation tissue samples and cultured for experiments. Human NP cells were treated with LPS and then exposed to LIPUS (15 mW/cm2, 30 mW/cm2 and 60 mW/cm2) for 20 min daily for 3 days to determine the appropriate intensity to inhibit the expression of the inflammatory factors TNF-α and IL-1β. The gene and protein expression of aggrecan, collagen II, MMP-3 and MMP-9 was measured by real‐time PCR and western blotting, respectively. The activity of the nuclear factor‐kappa B (NF‐κB) pathway was examined by western blotting and immunofluorescence. After pretreatment with the NF-κB inhibitor PDTC, the expression of TNF-α, IL-1β, MMP-3 and MMP-9 was measured by real‐time PCR. Results LIPUS at intensities of 15 mW/cm2, 30 mW/cm2 and 60 mW/cm2 inhibited LPS-induced NP cell expression of the inflammatory factors TNF-α and IL-1β, especially at 30 mW/cm2. LIPUS significantly upregulated the gene and protein expression of aggrecan and collagen II and downregulated the gene and protein expression of MMP-3 and MMP-9 in LPS-induced NP cells. The NF‐κB signaling pathway was inhibited by LIPUS through inhibiting the protein expression of p-P65 and the translocation of P65 into the nucleus in LPS-induced NP cells. In addition, LIPUS had similar effects as the NF-κB inhibitor PDTC by inhibiting the NF-κB signaling pathway, inflammation and catabolism in LPS-induced human degenerative nucleus pulposus cells. Conclusion LIPUS inhibited inflammation and catabolism through the NF‐κB pathway in human degenerative nucleus pulposus cells.

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Ferulic Acid Improves Depressive-Like Behavior in Prenatally-Stressed Offspring Rats via Anti-Inflammatory Activity and HPA Axis

International Journal of Molecular Sciences ◽

10.3390/ijms20030493 ◽

2019 ◽

Vol 20 (3) ◽

pp. 493 ◽

Cited By ~ 8

Author(s):

Xingxing Zheng ◽

Ying Cheng ◽

Yiwei Chen ◽

Yisong Yue ◽

Yingchun Li ◽

...

Keyword(s):

Protein Expression ◽

Ferulic Acid ◽

Hpa Axis ◽

Glucocorticoid Receptors ◽

Metabolic Diseases ◽

Inflammatory Activity ◽

Tnf Α ◽

Immobility Time ◽

Prenatally Stressed ◽

Anti Inflammatory

Prenatal stress (PS) can increase the risk of nervous, endocrine and metabolic diseases, and immune dysfunction. Ferulic acid (FA) is a dietary phenolic acid that has pharmacological properties, including potent anti-inflammatory action. We used male, prenatally-stressed offspring rats to investigate the anti-depressive-like effects and possible anti-inflammatory mechanism of FA. We determined the animal behaviors, and the mRNA expression and concentration of inflammatory cytokines, and HPA axis. In addition, we assessed the modulation of hippocampal nuclear factor-κB (NF-κB) activation, neuronal nitric oxide synthase (nNOS) and glucocorticoid receptors (GR) expression via western blotting and immunohistochemistry. Administration of FA (12.5, 25, and 50 mg/kg/day, i.g.) for 28 days markedly increased sucrose intake, and decreased immobility time and total number of crossings, center crossings, rearing, and grooming in the male PS offspring. FA significantly reduced IL-6, IL-1β, and TNF-α concentration and increased IL-10 concentration in male, prenatally-stressed offspring, stimulated by the NF-κB pathway. In addition, FA inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), and increased interleukin-10 (IL-10) mRNA and protein expression. Furthermore, FA markedly decreased the serum adrenocorticotropin (ACTH) and corticosterone concentration by the increase of GR protein expression. Taken together, this study revealed that FA has anti-depressive-like effects in male, prenatally-stressed offspring, partially due to its anti-inflammatory activity and hypothalamic-pituitary-adrenal (HPA) axis.

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Prolonged Chronic Consumption of a High Fat with Sucrose Diet Alters the Morphology of the Small Intestine

International Journal of Molecular Sciences ◽

10.3390/ijms22147280 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7280

Author(s):

Roberta Sferra ◽

Simona Pompili ◽

Alfredo Cappariello ◽

Eugenio Gaudio ◽

Giovanni Latella ◽

...

Keyword(s):

Small Intestine ◽

Leptin Receptor ◽

Eating Habits ◽

Standard Diet ◽

High Fat ◽

Ppar Γ ◽

Starting Point ◽

Tnf Α ◽

Sucrose Diet ◽

Inflammatory Molecules

(1) The high-fat diet (HFD) of western countries has dramatic effect on the health of several organs, including the digestive tract, leading to the accumulation of fats that can also trigger a chronic inflammatory process, such as that which occurs in non-alcohol steatohepatitis. The effects of a HFD on the small intestine, the organ involved in the absorption of this class of nutrients, are still poorly investigated. (2) To address this aspect, we administered a combined HFD with sucrose (HFD w/Suc, fat: 58% Kcal) regimen (18 months) to mice and investigated the morphological and molecular changes that occurred in the wall of proximal tract of the small intestine compared to the intestine of mice fed with a standard diet (SD) (fat: 18% Kcal). (3) We found an accumulation of lipid droplets in the mucosa of HFD w/Suc-fed mice that led to a disarrangement of mucosa architecture. Furthermore, we assessed the expression of several key players involved in lipid metabolism and inflammation, such as perilipin, leptin, leptin receptor, PI3K, p-mTOR, p-Akt, and TNF-α. All these molecules were increased in HFD mice compared to the SD group. We also evaluated anti-inflammatory molecules like adiponectin, adiponectin receptor, and PPAR-γ, and observed their significant reduction in the HFD w/Suc group compared to the control. Our data are in line with the knowledge that improper eating habits present a primary harmful assault on the bowel and the entire body’s health. (4) These results represent a promising starting point for future studies, helping to better understand the complex and not fully elucidated spectrum of intestinal alterations induced by the overconsumption of fat.

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Ligustrazine Attenuates Gastric Inflammation and Apoptosis in Helicobacter pylori-induced Gastric Epithelial Cells

Jundishapur Journal of Microbiology ◽

10.5812/jjm.116612 ◽

2021 ◽

Vol 14 (4) ◽

Author(s):

Yongjian Li ◽

Qiong Chen ◽

Shasha Wang ◽

Shichao Zhang

Keyword(s):

Helicobacter Pylori ◽

Epithelial Cells ◽

Protein Expression ◽

Cell Line ◽

Inflammatory Factors ◽

Pcr Analysis ◽

Epithelial Cell Line ◽

Gastric Epithelial Cells ◽

Tnf Α ◽

H Pylori

Background: Stomach disorders, including gastric cancer and gastritis, are associated with the pathogenic bacterium Helicobacter pylori. Enhanced inflammation is the characteristic of H. pylori-induced gastritis. Ligustrazine exerts anti-inflammatory properties in mouse asthma models and acute kidney injury. Objectives: To determine the role of ligustrazine in H. pylori-induced gastritis. Methods: Normal gastric epithelial cell line (GES-1) was cultured with H. pylori at a multiplicity of infection (MOI) of 100: 1 for 24 hours. GES-1 cell line under H. pylori condition was incubated with 100 or 200 μM ligustrazine for 24 hours. Cell viability and apoptosis were investigated by MTT and flow cytometry assays, respectively. Inflammation was assessed by determining the levels and mRNA expression of interleukins (IL)-6/8, tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein 1 (MCP-1) using ELISA and qRT-PCR analysis, respectively. Results: Helicobacter pylori infection reduced the viability and promoted the apoptosis of GES-1 cell line, accompanied by the enhanced activities of caspases 3 and 9. However, ligustrazine reversed the H. pylori-induced infection decreased viability, while increased apoptosis and caspases 3/9 activities in GES-1 cell line. Moreover, ligustrazine attenuated H. pylori-induced secretions of pro-inflammatory factors, IL-6/8, TNF-α, and MCP-1, in GES-1 cell line. The protein expression of inhibitor of NF-κB (IκBα) was downregulated in GES-1 cell line after H. pylori infection, while the protein expression levels of p65 and phosphorylation of IκBα were upregulated by H. pylori infection. On the contrary, ligustrazine decreased H. pylori-induced protein expression of IκBα, whereas increased protein expression of p65 and phosphorylation of IκBα. Conclusions: Ligustrazine exerted protective effects on H. pylori-induced gastric epithelial cells through inhibition of gastric inflammation and apoptosis and inactivation of NF-κB pathway.

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Molecular mechanisms of insulin resistance in normal pregnancy and gestational diabetes

Shidnoevropejskij zurnal vnutrisnoi ta simejnoi medicini ◽

10.15407/internalmed2021.01.022 ◽

2021 ◽

Vol 2021 (1) ◽

pp. 22-30

Author(s):

L.V. Zhuravlyova ◽

◽

N.V. Sokolnikova ◽

T.A. Rogachova ◽

◽

...

Keyword(s):

Insulin Resistance ◽

Gestational Diabetes ◽

Molecular Mechanisms ◽

Normal Pregnancy ◽

Inflammatory Factors ◽

Ppar Γ ◽

Tnf Α ◽

Therapeutic Measures ◽

Glut 4 Translocation ◽

Further Development

The purpose of this review article is to analyze current information on the molecular mechanisms of gestational diabetes and the prospects for their use in the further development of new effective treatments for this common pathology. Decreased ability of insulin to bind to its receptor, decreased IRS-1 expression and GLUT-4 translocation, and increased levels of p85α-PI-3 kinase subunits are involved in the development of insulin resistance during pregnancy. In gestational diabetes, there are not only more significant changes of the above mentioned indicators, but also increased levels of pro-inflammatory factors: TNF-α, IL-6, leptin and decreased insulin-sensitizing factors: adiponectin and PPAR-γ. Therapeutic measures aimed at normalizing the secretion of cytokines and adipokines reduce the risk of gestational diabetes mellitus and its complications and require further development

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Protection of Ang1-7 througth MKK/P38MAPKs inflammatory signal pathway on TNF-α stimulated mouse HL-1 cells

10.21203/rs.3.rs-1064422/v1 ◽

2021 ◽

Author(s):

Xuewen Wang ◽

Yuan Cao ◽

Pradeep depark ◽

Deepark Sharma ◽

Guangping Li ◽

...

Keyword(s):

Protein Expression ◽

Signal Pathway ◽

Inflammatory Factors ◽

Control Group ◽

Inflammatory Factor ◽

Tnf Α ◽

Significant Difference ◽

Atrial Myocyte ◽

Group B ◽

Group Control Group

Abstract Background to explore the effect of Ang1-7 througth MKK/P38MAPKs inflammatory signaling pathway on TNF-α-stimulated mouse HL-1 cells. Methods Using TNF-α (100 µg/ml) to establish an inflammatory atrial fibrillation model in HL-1 cell, which derived from mouse atrial myocyte. treated HL-1 cells with different concentrations of Ang 1-7 (0.1, 1 and 10 mmol/L) and divided into 5 groups, namely A group(control group), B group(TNF ), C group(TNF + Ang 1-7 0.1 mmol/L), D group(TNF + Ang 1-7 1 mmol/L ) and E group(TNF + Ang 1-7 10 mmol/L ). Firstly, different concentrations of Ang 1-7 (0.1 mmol/L, 1 mmol/L and 10 mmol/L) were used to stimulate for half an hour, and then TNF-α (100 µg/ml) was added to stimulate for four hours. Both the cells and supernatant were collected. Cells were collected for Western Blotting to detect the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38. The supernatant was subjected to flow cytometry for detecting multi-inflammatory factors. Results Compared with the A group, the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38 was statistically significant increased after stimulation with inflammatory factors (TNF-α) (P < 0.05). After intervention with Ang 1-7, the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38 was statistically significant lower than that of B group (P < 0.05). There is no significant difference of the protein expression of P38 after stimulation with inflammatory factor (TNF-α). Compared with the A group, there was no significant difference in the protein expression of MAS after the stimulation of inflammatory factor (TNF-α). After the intervention of Ang 1-7, the protein expression of MAS was higher than that of the A group and B group, but there was no significant difference (P > 0.05). The expression of MAS protein had an increasing trend, but there was no significant difference (P > 0.05). TGF-β, TNF-α was significantly increased after stimulating factor (TNF-α) was given, but was decreased after the intervention of Ang 1-7, both there were statistically significant (P < 0.05). IL-6 also had the same trend, but there was no significant difference. Conclusion Ang1-7 througth MKK/P38MAPKs inflammatory signal pathway protected on TNF-α stimulated mouse HL-1 cells

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Loki Zupa alleviates inflammatory and fibrotic responses in cigarette smoke induced rat model of chronic obstructive pulmonary disease

10.21203/rs.3.rs-24856/v1 ◽

2020 ◽

Author(s):

Nabijan Mohammadtursun ◽

Qiuping Li ◽

Muhammadjan Abuduwaki ◽

Shan Jiang ◽

Hu Zhang ◽

...

Keyword(s):

Protein Expression ◽

Blood Serum ◽

Cigarette Smoke ◽

Rat Model ◽

Lavage Fluid ◽

Inflammatory Factors ◽

Chronic Obstructive ◽

Model Group ◽

Tnf Α ◽

Bronchial Alveolar Lavage Fluid

Abstract BackgroundLoki zupa formula is kind of a traditional medicines which used to treat airway diseases, especially those caused by abnormal phlegm, such as cough, asthma and chronic bronchitis. The study was to explore the anti-inflammatory and anti-remodeling effects of Loki zupa using a cigarette-smoke induced rat model of chronic obstructive pulmonary disease.MethodsThe rats were divided into five groups: the normal group, the model group, the LZ 4 g/kg and LZ8g/kg group, and the positive control group. Rats were exposed to cigarette smoke for 24 weeks to induce a COPD rat model. Lung function was assessed. Histopathological changes were recorded using Haematoxylin-eosin. Mucus hypersecretion was evaluated by PAS staining. Inflammatory factors were measured in blood serum and bronchial alveolar lavage fluid using an enzyme-linked immunosorbent assay. Malondialdehyde and superoxide dismutase and glutathione S—transferase levels were tested by biochemical methods. Gene expression patterns were evaluated using GN-GeneChip Clariom S Array for rat from Affymetrix. And top upregulated and downregulated genes validated by qPCR. And these genes was also compared with gene transcriptomic data from smoker patients with emphysema and non-smokers in GEO dataset. IL-6/PLAGA2A signalling protein expression was assessed by western blot and immunohistochemistry. TGF-β1and smad2/3 signalling expressions were analysed by western Blot.Results Loki zupa improved COPD rats lung function as compared to the model group and pathological changes including inflammatory cell infiltration and goblet cell metaplasia was alleviated in rats treated with Loki zupa . Inflammatory factors IL-6, TNF-α, IL-1β and TGF-β1 decreased while significant increase was observed in blood serum IL-10 content in rats treated with Loki zupa . And IL-6 and TNF-α level in bronchial alveolar lavage fluid showed same expression trend in blood serum, while there was no change in MMP-9 content. It also increased antioxidant enzyme SOD activity while reducing the lipid peroxidation. Gene microarray analysis showed there were 355 differentially expressed gene in LZ treated COPD rat lung as compared to model group. Both microarray and qPCR results showed that top differentially expressed genes nxt1(up regulated ) and pla2g2a (down regulated) expression were also reversed by LZ treatment. And protein expression level of IL-6 and pla2g2a was also elevated in CS exposed rats while significant reduction was observed in LZ treated rats. Accordingly, Loki zupa inhibited Collagen-1 upstream protein expression of TGF-β/smad2/3 signalling pathway. Conclusion These results demonstrated that Loki zupa showed protective effects in the lung of the COPD rat model. This mainly because of Loki zupa exerts anti-inflammatory effects by blocking IL-6/pla2g2a signalling and inhibiting inflammatory gene expression and attenuates fibrotic responses by inhibiting TGF-β/smad2/3 signalling pathway.

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T-614 attenuates knee osteoarthritis via regulating Wnt/β-catenin signaling pathway

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02530-2 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Shan Cong ◽

Yan Meng ◽

Lingrui Wang ◽

Jiao Sun ◽

Ta bu shi·Nu er xia ti ◽

...

Keyword(s):

Articular Cartilage ◽

Protein Expression ◽

Knee Osteoarthritis ◽

Signaling Pathway ◽

Underlying Mechanism ◽

Cartilage Tissue ◽

Inflammatory Factors ◽

Dependent Manner ◽

Tnf Α ◽

Mrna And Protein Expression

Abstract Background The aim of this study was to investigate the effect of Iguratimod (T-614) on rat knee osteoarthritis (KOA) and further to explore its underlying mechanism. Methods In this study, papain-induced KOA model was constructed. Hematoxylin and eosin (H&E) staining was conducted to observe the pathological changes of cartilage tissue and Mankin scoring principle was used for quantitative scoring. Transmission electron microscopy (TEM) was applied to observe the ultrastructure of cartilage tissue. ELISA was used to measure the levels of matrix metalloproteinase 13 (MMP-13) and inflammatory factors (interleukin (IL)-6 and tumor necrosis factor a (TNF-a)) in serum. RT-qPCR and immunohistochemistry were conducted to detect mRNA expression and protein expression of key genes in Wnt/β-catenin pathway. Results H&E, Mankin scoring, and TEM data confirmed that compared with model group, T-614 significantly improved the degeneration of articular cartilage. Besides, we observed that low, middle, and high doses of T-614 could decrease the levels of MMP13, TNF-α, and IL-6 in serum to different degrees. Mechanically, T-614 downregulated the mRNA and protein expression of β-catenin and MMP13 in cartilage tissue via a dose-dependent manner, and on the contrary upregulated the mRNA and protein expression of glucogen synthase kinase-3 beta (GSK-3β). Conclusion Our results suggested that T-614 can reduce the level of its downstream target gene MMP-13 and downregulate the expression of inflammatory cytokines TNF-α and IL-6 by regulating the Wnt/β-catenin signaling pathway, thereby inhibiting joint inflammation and controlling KOA degeneration of articular cartilage.

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Pirfenidone attenuates synovial fibrosis and postpones the progression of osteoarthritis by anti-fibrotic and anti-inflammatory properties in vivo and in vitro

Journal of Translational Medicine ◽

10.1186/s12967-021-02823-4 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Qilu Wei ◽

Ning Kong ◽

Xiaohui Liu ◽

Run Tian ◽

Ming Jiao ◽

...

Keyword(s):

Protein Expression ◽

Cell Counting ◽

Enzyme Linked Immunosorbent Assay ◽

Fast Green ◽

Expression Levels ◽

Tnf Α ◽

Anti Inflammatory ◽

Safranin O ◽

Tgf Β1

Abstract Background Osteoarthritis (OA) is a disease of the entire joint involving synovial fibrosis and inflammation. Pathological changes to the synovium can accelerate the progression of OA. Pirfenidone (PFD) is a potent anti-fibrotic drug with additional anti-inflammatory properties. However, the influence of PFD on OA is unknown. Methods Proliferation of human fibroblast-like synoviocytes (FLSs) after treatment with TGF-β1 or PFD was evaluated using a Cell Counting Kit-8 assay and their migration using a Transwell assay. The expression of fibrosis-related genes (COL1A1, TIMP-1, and ACTA-2) and those related to inflammation (IL-6 and TNF-α) was quantified by real-time quantitative PCR. The protein expression levels of COL1A1, α-SMA (coded by ACTA-2), IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay. A rabbit model of OA was established and then PFD was administered by gavage. The expression of genes related to fibrosis (COL1A1, TIMP-1, and ADAM-12) and inflammation (IL-6 and TNF-α) was measured using RNA extracted from the synovium. Synovial tissue was examined histologically after staining with H&E, Masson’s trichrome, and immunofluorescence. Synovitis scores, the volume fraction of collagen, and mean fluorescence intensity were calculated. Degeneration of articular cartilage was analyzed using a Safranin O-fast green stain and OARSI grading. Results The proliferation of FLSs was greatest when induced with 2.5 ng/ml TGF-β1 although it did not promote their migration. Therefore, 2.5 ng/ml TGF-β1 was used to stimulate the FLSs and evaluate the effects of PFD, which inhibited the migration of FLSs at concentrations as low as 1.0 mg/ml. PFD decreased the expression of COL1A1 while TGF-β1 increased both mRNA and protein expression levels of IL-6 but had no effect on α-SMA or TNF-α expression. PFD decreased mRNA expression levels of COL1A1, IL-6, and TNF-α in vivo. H&E staining and synovitis scores indicated that PFD reduced synovial inflammation, while Masson’s trichrome and immunofluorescence staining suggested that PFD decreased synovial fibrosis. Safranin O-Fast Green staining and the OARSI scores demonstrated that PFD delayed the progression of OA. Conclusions PFD attenuated synovial fibrosis and inflammation, and postponed the progression of osteoarthritis in a modified Hulth model of OA in rabbits, which was related to its anti-fibrotic and anti-inflammatory properties.

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Very Early Exercise Rehabilitation After Intracerebral Hemorrhage Promotes Inflammation in the Brain

Neurorehabilitation and Neural Repair ◽

10.1177/15459683211006337 ◽

2021 ◽

pp. 154596832110063

Author(s):

Keigo Tamakoshi ◽

Madoka Maeda ◽

Shinnosuke Nakamura ◽

Nae Murohashi

Keyword(s):

Intracerebral Hemorrhage ◽

Protein Expression ◽

Brain Regions ◽

Motor Dysfunction ◽

Inflammatory Factors ◽

Mrna Levels ◽

Exercise Rehabilitation ◽

Early Exercise ◽

Polymerase Chain ◽

To Receive

Background Very early exercise has been reported to exacerbate motor dysfunction; however, its mechanism is largely unknown. Objective This study examined the effect of very early exercise on motor recovery and associated brain damage following intracerebral hemorrhage (ICH) in rats. Methods Collagenase solution was injected into the left striatum to induce ICH. Rats were randomly assigned to receive placebo surgery without exercise (SHAM) or ICH without (ICH) or with very early exercise within 24 hours of surgery (ICH+VET). We observed sensorimotor behaviors before surgery, and after surgery preexercise and postexercise. Postexercise brain tissue was collected 27 hours after surgery to investigate the hematoma area, brain edema, and Il1b, Tgfb1, and Igf1 mRNA levels in the striatum and sensorimotor cortex using real-time reverse transcription polymerase chain reaction. NeuN, PSD95, and GFAP protein expression was analyzed by Western blotting. Results We observed significantly increased skillful sensorimotor impairment in the horizontal ladder test and significantly higher Il1b mRNA levels in the striatum of the ICH+VET group compared with the ICH group. NeuN protein expression was significantly reduced in both brain regions of the ICH+VET group compared with the SHAM group. Conclusion Our results suggest that very early exercise may be associated with an exacerbation of motor dysfunction because of increased neuronal death and region-specific changes in inflammatory factors. These results indicate that implementing exercise within 24 hours after ICH should be performed with caution.

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