scholarly journals Relationship between Pain Behavior and Changes in KCNA2 Expression in the Dorsal Root Ganglia of Rats with Osteoarthritis

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Qihong Zhao ◽  
Lei Fan ◽  
Jiafeng Wang ◽  
Xiaoming Deng
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Saline Group ◽  
Pain Behavior ◽  
Control Group ◽  
Sprague Dawley ◽  
Blank Control Group ◽  
Cartilage Surface ◽  
Gated Channel ◽  
Surface Destruction

Objective. To investigate the relationship between pain behavior and potassium voltage-gated channel subfamily A member 2 (KCNA2) expression in dorsal root ganglia (DRGs) of rats with osteoarthritis (OA). Methods. Male Sprague-Dawley rats were randomly divided into three groups: blank control group (group C), normal saline group (group S), and group OA. Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured one day before injection and one, two, four, and six weeks after injection. At one, two, four, and six weeks after injection, pathological knee joint changes and activated transcription factor-3 (ATF-3) and KCNA2 expressions in DRGs were analyzed. Results. Compared with preinjection, PWMT and PWTL at two, four, and six weeks after injection were significantly decreased in the group OA (P<0.05 or 0.01). Compared with group C, PWMT and PWTL at two, four, and six weeks after injection were significantly decreased in the group OA (P<0.05 or 0.01). In the group OA, slight local articular cartilage surface destruction was found at week one. The cartilage surface destruction gradually developed, and the exacerbation of cartilage matrix reduction and bone hyperplasia were increasingly aggravated and eventually evolved into advanced OA in the second to sixth weeks. Compared with group C, ATF-3 expression was significantly increased, and KCNA2 expression was significantly decreased in the group OA at two, four, and six weeks after injection (P<0.05 or 0.01). Compared to baseline, ATF-3 expression was significantly increased, and KCNA2 expression was significantly decreased in the group OA (P<0.05 or 0.01). Conclusion. Pain behavior in OA rats was associated with decreased KCNA2 expression in DRGs.

scholarly journals Oral Pyruvate Protection of Dorsal Root Ganglia  in Simulated Weightlessness Rats

2020 ◽  
Author(s):  
Yuan Li ◽  
Heng Zhang ◽  
Ning-Tao Ren ◽  
Chao Chen ◽  
Peng Qi ◽  
...  
Keyword(s):  
Dorsal Root Ganglia ◽  
Normal Saline ◽  
Dorsal Root ◽  
Morphological Changes ◽  
Saline Group ◽  
Organ Injury ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
And Function

Abstract Background: Previous studies demonstrate that long-tern microgravity induces multi-organ injury and dysfunction, including the dorsal root ganglia (DRG) damage. This study investigated oral pyruvate protective effects on lumbar 5 (L5) DRG nerve tissues in rats subjected to hindlimb unweighting (HU).Results: Male Sprague-Dawley rats were randomly assigned to four groups (n=10): control group (Group CON), suspension group (Group SUS), normal saline group (Group SAL) and sodium pyruvate group (Group PYR), respectively. The rats of SUS, SAL and PYR groups were simulated with microgravity by tail suspension of HU for 8 weeks. Rats in Groups SAL and PYR fed with normal saline and pyruvate saline, respectively. Histopathological and immunofluorescence examinations were conducted and levels of glial cell line-derived neurotrophic factor (GDNF), glial fibrillary acidic protein (GFAP), ATP and ATPase were measured in DRG tissues; L5 spinal cord scans were also carried out in rats following HU. Results showed that the HU resulted in significant alterations in DRG nerve tissues’ structure and function in Groups SUS and SAL, whereas morphological changes were not significantly distinguished between Group PYR and Group CON; GDNF, GFAP, ATP and ATPase levels were mostly preserved in Group PYR, but still worse than in Group CON. The significance of oral pyruvate protection against DRG injury following HU and the dose and formula of oral pyruvate solutions were discussed for use in astronauts’ spaceflight.Conclusions: oral pyruvate effectively protected L5 DRG from pathological alterations and dysfunction induced by the HU in rats. Further studies and clinical trials are warranted.

scholarly journals Pentoxifylline Ameliorates Mechanical Hyperalgesia in a Rat Model of ChemotherapyInduced Neuropathic Pain

2016 ◽  
Vol 4;19 (4;5) ◽  
pp. E589-E600
Author(s):  
Salahadin Abdi
Keyword(s):  
Neuropathic Pain ◽  
Continuous Infusion ◽  
Inflammatory Cytokines ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Pain Treatment ◽  
Phosphodiesterase Inhibitor ◽  
Pain Behavior ◽  
Sprague Dawley ◽  
Tnf Α

Background: Chemotherapy-induced neuropathic pain is difficult to treat. Pentoxifylline inhibits the production of inflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). Objective: The aims of our study were to investigate the analgesic and preventive effects of pentoxifylline on paclitaxel-induced neuropathic pain in rats and to identify its mechanisms of action. Study Design: Controlled animal study. Methods: Neuropathic pain was induced with intraperitoneally injected paclitaxel on 4 alternate days in male Sprague-Dawley rats. Pentoxifylline was administered systemically as a single injection and a continuous infusion before or after the injection of paclitaxel. The mechanical threshold for allodynia was measured by using von Frey filaments. Protein levels and localization of inflammatory cytokines were performed by using Western blotting and immunohistochemistry, respectively. Results: After the rats developed neuropathic pain behavior, a single intraperitoneal injection and continuous infusion of pentoxifylline ameliorated paclitaxel-induced mechanical allodynia. In addition, systemic infusion of pentoxifylline in the early phase of the development of pain behavior delayed the onset of paclitaxel-induced pain behavior. Paclitaxel increased the levels of the catalytic subunit α of protein kinase A, phosphorylated nuclear factor κB, TNF-α, and IL-1β in the lumbar dorsal root ganglia. Pentoxifylline decreased the paclitaxel-induced TNF-α and IL1β levels. In addition, IL-1β was expressed in neurons and satellite cells in the lumbar dorsal root ganglia after paclitaxel. Limitations: Although this study was performed in the animal model by well-designed manner, clinical study will be needed to confirm the analgesic effect of pentoxifylline. Conclusion: Pentoxifylline alleviated chemotherapy-induced neuropathic pain in rats by reducing the levels of inflammatory cytokines in dorsal root ganglia and may be effective chemotherapyinduced neuropathic pain in patients. Key words: Chemotherapy, chronic pain, inflammatory cytokines, neuropathic pain, paclitaxel, pain behavior, pain treatment, pentoxifylline, phosphodiesterase inhibitor

scholarly journals Effects of Ozone on Hippocampus BDNF and Fos Expressions in Rats with Chronic Compression of Dorsal Root Ganglia

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lingling Zhu ◽  
Yanxiu Wang ◽  
Xiaowen Lin ◽  
Xu Zhao ◽  
Zhi jian Fu
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Sham Group ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Expression Levels ◽  
Fos Protein ◽  
Before And After ◽  
Formula Group ◽  
Fos Expression

The effects of ozone on hippocampal expression levels of brain-derived neurotrophic factor (BDNF) and c-fos protein (Fos) were evaluated in rats with chronic compression of dorsal root ganglia (CCD). Forty-eight adult female Sprague-Dawley rats were randomly divided into the following 4 groups ( n = 12 ): sham operation (sham group), CCD group, CCD with 20 μg/ml of ozone ( CCD + A O 3 group), and CCD with 40 μg/ml of ozone ( CCD + B O 3 group). Except the sham group, unilateral L5 dorsal root ganglion (DRG) compression was performed on all other groups. On days 1, 2, and 4 after the operation, the CCD + A O 3 and CCD + B O 3 groups were injected with 100 μl of ozone with concentrations of 20 and 40 μg/ml, respectively. Thermal withdrawal latencies (TWLs) and mechanical withdrawal thresholds (MWTs) were measured at various time points before and after the operation. BDNF and Fos expressions were examined in the extracted hippocampi using immunohistochemistry. The TWLs and MWTs of CCD model rats that received ozone were lower with decreased BDNF and increased Fos expression levels, on day 21 after the operation, compared to those of the sham group ( P < 0.05 ). The TWLs and MWTs of the CCD + A O 3 and CCD + B O 3 groups were higher with increased BDNF and decreased Fos expression levels, on day 21 after the operation, compared to those of the CCD group ( P < 0.05 ). The TWLs were longer and the MWTs were higher in the CCD + B O 3 group at each time point with increased BDNF and decreased Fos expression levels, on day 21 after the operation, compared to those of the CCD + A O 3 group ( P < 0.05 ). Our results revealed that ozone can relieve the neuropathic pain caused by the pathological neuralgia resulting from DRG compression in rats. The mechanism of action for ozone is likely associated with changes in BDNF and Fos expression levels in the hippocampus.

Microstructural changes and immunohistological analysis of pro-inflammatory cytokines in spleens of lipopolysaccharide-induced rats

2018 ◽  
Author(s):  
Y. B. Zhong ◽  
X. L. Zhang ◽  
M. Y. Lv ◽  
X. F. Hu ◽  
Y. Li
Keyword(s):  
Inflammatory Cytokines ◽  
Optical Density ◽  
Normal Saline ◽  
Interleukin 1 ◽  
Saline Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Lymphoid Follicles ◽  
Pro Inflammatory Cytokines

This study investigated splenic status changes in weaned Sprague-Dawley rats induced by lipopolysaccharide. There were forty 26-day-old rats selected randomly and equally divided into two groups. The treatment group received daily single doses of lipopolysaccharide, and the control group was treated with normal saline. We conducted haematoxylin-eosin staining, immunohistochemical staining and semi-quantitative optical density analysis for both groups on the 29th, 32nd, 35th and 38th days after treatment. The results indicated that splenic marginal zone in the lipopolysaccharide group was thinner or disappeared compared to that of the saline group. However, the periarterial lymphoid sheath and the diameters of splenic lymphoid follicles appeared thicker and wider than those in the saline group (P less than 0.05). The expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha was mainly localized within the periarterial lymphoid sheath and splenic lymphoid follicles in the lipopolysaccharide treated rats. The integrated optical density and the average optical density in the lipopolysaccharide group were greater than those in the normal saline treated group (P less than 0.05). In conclusion, splenic immune function is probably strengthened by altering microstructures and releasing pro-inflammatory cytokines following lipopolysaccharide treatment.

Effect of Electro-acupuncture on Ultrastructure in Diabetic Gastroparesis Model Rats

2015 ◽  
Vol 3 (1) ◽  
pp. 70-76
Author(s):  
Feng-E He ◽  
Quan-Quan Wan ◽  
Yan Peng ◽  
Ya-Ping Lin ◽  
Jing Shen
Keyword(s):  
Smooth Muscle ◽  
Point Group ◽  
Diabetic Gastroparesis ◽  
Control Group ◽  
Therapeutic Effects ◽  
Phenol Red ◽  
Model Group ◽  
Sprague Dawley ◽  
Blank Control Group ◽  
Gastric Emptying Rate

Abstract Objective: To observe the effects of electro-acupuncture (EA) on ultrastructure of gastric antrum smooth muscle cells (GASMCs) in diabetic gastroparesis (DGP) model rats, and to explore the possible mechanism underlying the therapeutic effects of EA. Methods: Sixty Sprague Dawley rats were randomly divided into 5 groups: blank control (group A), DGP model (group B), EA point (group C), EA non-point (group D), Metoclopramide control (group E). DGP rat model was established by 2% STZ intraperitoneal injection at once, and then being fed with high-sugar-high-fat (HSHF) for 8wks. Phenol red lavage method was employed to measure gastric emptying rate (GER) and intestinal migration rate (IMR). The ultrastructure of GASMCs was observed under the electronic microscope. Results: Compared with the blank control group, the GER and IMR in model group were decreased significantly (P＜0.05 or P＜0.01). Compared with the model group, the GER and IMR in EA point group were increased significantly(P＜0.05 or P＜0.01). Electro-acupuncture on “Zu San Li”(ST36) point, etc. has been observed improving the ultrastructure of GASMCs, as well as increasing the number of interstitial cells of Cajal (ICCs). Conclusion: Electro-acupuncture can improve the GI motility promisingly, based on a potential underlying mechanism that the electro-acupuncture can improve the ultrastructure of gastric smooth muscle, and increase the number of ICCs.

Expression of calcium/calmodulin-dependent protein kinase II in dorsal root ganglia in diabetic rats 6 months and 1 year after diabetes induction

2013 ◽  
Vol 4 (4) ◽  
pp. 259-259
Author(s):  
L. Ferhatovic ◽  
A. Jelicic ◽  
M. Boric ◽  
A. Banozic ◽  
D. Sapunar ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Dorsal Root ◽  
Control Group ◽  
Type I ◽  
Sprague Dawley ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein ◽  
Diabetes Induction

Abstract Aim The aim of this study was to compare expression of total calcium/calmodulin-dependent protein kinase II (tCaMKII) and its α, β, γ and δ isoforms in dorsal root ganglion (DRG) in rat models of diabetes mellitus type I (DM1), 6 months and 1 year after diabetes induction. Methods A total of 45 male Sprague-Dawley rats weighing 160-200 g were assigned into four experimental groups: 6-months DM1 and its control group, 1-year and its control group. For the induction of DM1, after overnight fasting animals were injected intraperitonealy with 55 mg/kg of the streptozotocine (STZ). Rats were sacrificed 6 months and 1 year after the diabetes induction. The L4 and L5 ganglions were removed, fixed, embedded in freezing medium and sectioned on a cryostat. Immunofluorescence analysis was performed for detection of tCaMKII and its α, β, γ and δ isoforms. Image J software was used for analysis of immunofluorescence. Results The diabetes was successfully induced as confirmed by measurement of glucose levels and weight increase. Analysis of tCaMKII expression in DRGs revealed no differences between DM1 and control animals after 6 and 12 months. In diabetic animals, the expression of α and β isoforms decreased significantly after 6 months, compared to the controls, while decrease of γ and δ was observed after one year of diabetes in diabetic animals. Conclusions The observed changes in the expression of CaMKII isoforms reveal plastic changes of this enzyme during the chronic diabetic state and may be involved in the chronic neuropathic pain development.

scholarly journals Astragalin Alleviates Neuropathic Pain by Suppressing P2X4-Mediated Signaling in the Dorsal Root Ganglia of Rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Mengke Wang ◽  
Xia Cai ◽  
Yueying Wang ◽  
Shizhen Li ◽  
Na Wang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Therapeutic Potential ◽  
Purinergic Receptor ◽  
Pain Behavior ◽  
Hek293 Cells ◽  
Protective Effects ◽  
Satellite Glial Cell ◽  
Clinical Pain

Neurologic damage often leads to neuropathic pain, for which there are no effective treatments owing to its complex pathogenesis. The purinergic receptor P2X4 is closely associated with neuropathic pain. Astragalin (AST), a compound that is used in traditional Chinese medicine, has protective effects against allergic dermatitis and neuronal injury, but its mechanism of action is not well understood. The present study investigated whether AST can alleviate neuropathic pain in a rat model established by chronic constriction injury (CCI) to the sciatic nerve. The model rats exhibited pain behavior and showed increased expression of P2X4 and the activated satellite glial cell (SGC) marker glial fibrillary acidic protein in dorsal root ganglia (DRG). AST treatment partly abrogated the upregulation of P2X4, inhibited SGC activation, and alleviated pain behavior in CCI rats; it also suppressed ATP-activated currents in HEK293 cells overexpressing P2X4. These data demonstrate that AST relieves neuropathic pain by inhibiting P2X4 and SGC activation in DRG, highlighting its therapeutic potential for clinical pain management.

Effects of uranium depletion on 1α-hydroxylase in kidney of rats

2010 ◽  
Vol 30 (7) ◽  
pp. 786-790 ◽  
Author(s):  
Minfen Yan ◽  
Gaoren Zhong ◽  
Linfeng Gao ◽  
Xiqiao Xia ◽  
Lihua Wang ◽  
...  
Keyword(s):  
Active Form ◽  
Underlying Mechanism ◽  
Biologically Active ◽  
Control Group ◽  
High Dose ◽  
Sprague Dawley ◽  
Blank Control Group ◽  
Sprague Dawley Rats ◽  
Dose Levels ◽  
Medium Dose

This study was designed to evaluate the effects of depleted uranium (DU) on 1α-hydroxylase in the kidney of rats and to delinerate the mechanism of damage to kidneys and bones by DU. Male Sprague-Dawley rats were surgically implanted with DU fragments at three dose levels (0.1 g, 0.2 g and 0.3 g). After 3, 6 or 12 months, the concentration of 1α,25(OH)2D3 in the kidney was measured by radioimmunoassay. The activity of 1α-hydroxylase was shown by the production of 1α,25(OH)2D3 after incubation. The results showed that the 1α-hydroxylase activity in the kidney was decreased after 3 months (27.2% at the medium dose DU group, p < 0.05; 33.4% at the high dose DU group, p < 0.01). In contrast, at 6 months and 12 months after implantation of DU, the activity of renal 1α-hydroxylase in DU-treated animals was not decreased significantly in comparison with the controls (p > 0.05). On the other hand, the activity of renal 1α-hydroxylase was decreased by 33.1% (p < 0.05) and 34.4% (p < 0.01) in blank control groups at 6 and 12 months, respectively, when compared with the blank control group at 3 months. In conclusion, this study showed that chronic DU exposure could induce renal damages and inhibit the synthesis of biologically active form of vitamin D, which may be the underlying mechanism of bone metabolic disorder caused by renal injury after DU exposure.

scholarly journals Metformin improves monosodium-iodoacetate-induced osteoarthritis via regulation of pain mediators and autophagy-lysosomal pathway.

2020 ◽  
Author(s):  
Hyun Sik Na ◽  
Ji Ye Kwon ◽  
Seung Hoon Lee ◽  
Seon-young Lee ◽  
KyungAh Jung ◽  
...  
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Cartilage Damage ◽  
The Elderly ◽  
Cartilage Destruction ◽  
Control Group ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Monosodium Iodoacetate ◽  
And Cartilage

Abstract Background Osteoarthritis (OA) is the most common degenerative arthritis associated with pain and cartilage destruction in the elderly. Its pathogenesis involves inflammatory pathways. Metformin is used to treat type 2 diabetes but also exhibits regulation of autophagy pathway. This study investigated the ability of metformin to ameliorate the severity of monosodium iodoacetate (MIA)-induced OA in rats. Methods Metformin was administered orally every day to rats with OA experimentally induced by intra-articular injection of MIA. Paw-withdrawal latency and threshold were used to assess pain severity. Cartilage damage and pain mediators in dorsal root ganglia were evaluated by histological analysis and a scoring system. Relative mRNA expression was measured by real-time PCR. Results Metformin ameliorated the progression of experimental OA and exhibited both anti-nociceptive properties and cartilage protection. The metformin-induced down-regulation of pain mediators, including CGRP, in dorsal root ganglia and protection against bone damage were also determined. In chondrocytes from OA patients, metformin decreased expression of genes encoding catabolic factors stimulated by interleukin-1β and inflammatory cell death factors and induced autophagosome–lysosome fusion phenotype. The combination therapy of metformin and celecoxib had significantly less cartilage damage than either the metformin alone group or the control group. Conclusions These results imply the possibility of therapeutic use of metformin in OA patients, based on its ability to suppress pain and protect cartilage.

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