scholarly journals Antinociceptive Effect ofCyperi rhizomaandCorydalis tuberExtracts on Neuropathic Pain in Rats

2012 ◽  
Vol 16 (6) ◽  
pp. 387 ◽  
Author(s):  
Jae-Gyun Choi ◽  
Suk-Yun Kang ◽  
Jae-Min Kim ◽  
Dae-Hyun Roh ◽  
Seo-Yeon Yoon ◽  
...  
2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Yan Dong ◽  
Chong-Yang Li ◽  
Xiao-Min Zhang ◽  
Ya-Nan Liu ◽  
Shuang Yang ◽  
...  

AbstractOur previous research has shown that galanin plays an antinociceptive effect via binding to galanin receptors (GalRs) in nucleus accumbens (NAc). This study focused on the involvement of GalR2 in galanin-induced antinociceptive effect in NAc of neuropathic pain rats. The chronic constriction injury of sciatic nerve (CCI) was used to mimic neuropathic pain model. The hind paw withdrawal latency (HWL) to thermal stimulation and hind paw withdrawal threshold (HWT) to mechanical stimulation were measured as the indicators of pain threshold. The results showed that 14 and 28 days after CCI, the expression of GalR2 was up-regulated in bilateral NAc of rats, and intra-NAc injection of GalR2 antagonist M871 reversed galanin-induced increases in HWL and HWT of CCI rats. Furthermore, intra-NAc injection of GalR2 agonist M1145 induced increases in HWL and HWT at day 14 and day 28 after CCI, which could also be reversed by M871. Finally, we found that M1145-induced antinociceptive effect in NAc of CCI rats was stronger than that in intact rats. These results imply that the GalR2 is activated in the NAc from day 14 to day 28 after CCI and GalR2 is involved in the galanin-induced antinociceptive effect in NAc of CCI rats.


Pain ◽  
2011 ◽  
Vol 152 (10) ◽  
pp. 2224-2232 ◽  
Author(s):  
Gerusa Duarte Dalmolin ◽  
Cássia Regina Silva ◽  
Flávia Karine Rigo ◽  
Guilherme Monteiro Gomes ◽  
Marta do Nascimento Cordeiro ◽  
...  

2020 ◽  
Author(s):  
Josué Vidal Espinosa‐Juárez ◽  
Osmar Antonio Jaramillo‐Morales ◽  
Myrna Déciga‐Campos ◽  
Luis Alfonso Moreno‐Rocha ◽  
Francisco Javier López‐Muñoz

2003 ◽  
Vol 99 (2) ◽  
pp. 449-454 ◽  
Author(s):  
Dorien H. Vrinten ◽  
Willem Hendrik Gispen ◽  
Cor J. Kalkman ◽  
Roger A. H. Adan

Background The authors recently demonstrated that administration of the melanocortin-4 receptor antagonist SHU9119 decreased neuropathic pain symptoms in rats with a sciatic chronic constriction injury. The authors hypothesised that there is a balance between tonic pronociceptive effects of the spinal melanocortin system and tonic antinociceptive effects of the spinal opioid system. Therefore, they investigated a possible interaction between these two systems and tested whether opioid effectiveness could be increased through modulation of the spinal melanocortin system activity. Methods In chronic constriction injury rats, melanocortin and opioid receptor ligands were administered through a lumbar spinal catheter, and their effects on mechanical allodynia were assessed by von Frey probing. Results Naloxone (10-100 microg) dose-dependently increased allodynia (percent of maximum possible effect of -67 +/- 9%), which is in agreement with a tonic antinociceptive effect of the opioid system. SHU9119 decreased allodynia (percent of maximum possible effect of 60 +/- 13%), and this effect could be blocked by a low dose of naloxone (0.1 microg), which by itself had no effect on withdrawal thresholds. Morphine (1-10 microg) dose-dependently decreased allodynia (percent of maximum possible effect of 73 +/- 14% with the highest dose tested). When 0.5 microg SHU9119 (percent of maximum possible effect of 47 +/- 14%) was given 15 min before morphine, there was an additive antiallodynic effect of both compounds. Conclusions Together, these data confirm that there is an interaction between the spinal melanocortin and opioid systems and that combined treatment with melanocortin-4 receptor antagonists and opioids might possibly contribute to the treatment of neuropathic pain.


Author(s):  
Haritha Pasupulati ◽  
Satyanarayana S. V. Padi ◽  
Sujatha Dodoala ◽  
Prasad V. S. R. G. Koganti

Background: Paclitaxel-induced painful neuropathy is a major dose-limiting side effect and can persist for up to two years after completing treatment that greatly affects both the course of chemotherapy and quality of life in cancer patients. Peroxisome proliferator-activated receptor (PPAR)-γ belongs to a family of nuclear receptors known for their transcriptional and regulatory roles in metabolism, inflammation, and oxidative stress. However, the role of PPAR-γ activation on paclitaxel-induced neuropathic pain is not yet known. Objective: To investigate whether pioglitazone, a PPAR-γ agonist reduce paclitaxel-induced neuropathic pain and to elucidate underlying mechanisms. Methodology: Peripheral neuropathy was induced by administration of paclitaxel (2 mg/kg per injection) intraperitoneally on four alternate days (days 0, 2, 4, 6). Thermal hyperalgesia and mechanical allodynia were assessed and the markers of inflammation and nitroso-oxidative stress were estimated. Results: Pioglitazone did not induce hypoalgesia and had no effect on locomotor activity. Repeated oral administration of pioglitazone (10 and 20 mg/kg,) for 2 weeks started 14 days after paclitaxel injection markedly attenuated paw withdrawal responses to thermal (hyperalgesia) and mechanical (allodynia) stimuli. Further, pioglitazone administration significantly reduced elevated level of pro-inflammatory cytokine, TNF-α, in both the dorsal root ganglia and the spinal cord accompanied by marked decrease in oxidative stress parameters as well as increase in activity of antioxidant defense enzyme, superoxide dismutase, in the spinal cord after paclitaxel injection. Conclusion: The results of the present study demonstrate that pioglitazone, a PPAR-γ agonist exerted antinociceptive effect in paclitaxel-induced neuropathic pain through inhibiting neuroimmune inflammation in both the periphery and spinal cord and by reducing nitroso-oxidative stress in spinal cord. Our findings strongly suggest pharmacological activation of PPAR-g as a promising therapeutic target in paclitaxel-induced peripheral neuropathy and provide rationale for the clinical evaluation.


Polymers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 3837
Author(s):  
Rafaela Figueiredo Rodrigues ◽  
Juliana Barbosa Nunes ◽  
Sandra Barbosa Neder Agostini ◽  
Paloma Freitas dos Santos ◽  
Juliana Cancino-Bernardi ◽  
...  

This study offers a novel oral pregabalin (PG)-loaded drug delivery system based on chitosan and hypromellose phthalate-based polymeric nanocomposite in order to treat neuropathic pain (PG-PN). PG-PN has a particle size of 432 ± 20 nm, a polydispersity index of 0.238 ± 0.001, a zeta potential of +19.0 ± 0.9 mV, a pH of 5.7 ± 0.06, and a spherical shape. Thermal and infrared spectroscopy confirmed nanocomposite generation. PG-PN pharmacokinetics was studied after a single oral dose in male Wistar rats. PG-PN showed greater distribution and clearance than free PG. The antinociceptive effect of PG-PN in neuropathic pain rats was tested by using the chronic constriction injury model. The parameter investigated was the mechanical nociceptive threshold measured by the von Frey filaments test; PG-PN showed a longer antinociceptive effect than free PG. The rota-rod and barbiturate sleep induction procedures were used to determine adverse effects; the criteria included motor deficit and sedative effects. PG-PN and free PG had plenty of motors. PG-PN exhibited a less sedative effect than free PG. By prolonging the antinociceptive effect and decreasing the unfavorable effects, polymeric nanocomposites with pregabalin have shown promise in treating neuropathic pain.


2021 ◽  
Author(s):  
Lu Zhu ◽  
Hangping Zheng ◽  
Yaojing Jiang ◽  
Qi Zhang ◽  
Bin Lu ◽  
...  

Abstract Background: Spexin is implicated in multiple functions of energy metabolism and glucose homeostasis regulation. Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes and approximately half of the patients with DPN suffer from neuropathic pain. Recent experimental studies in mice have shown that Spexin has an antinociceptive effect, but there are no relevant reports in clinical studies. This study aimed to evaluate Spexin levels in people with painful DPN and controls and assess the correlation between serum Spexin levels and painful DPN.Methods: This is a cross-sectional study including 20 patients with diabetes but without DPN (non-DPN) as a control group, 24 patients with painless DPN, and 16 patients with painful DPN. Questionnaires and laboratory surveys were conducted to collect demographic and clinical data. The existence and severity of DPN were assessed using neurological symptom score, neurological examination, and electromyography. Serum Spexin levels were measured by ELISA. Results: Serum Spexin levels of patients with painful DPN were significantly lower than those of non-DPN patients (p<0.001) and painless DPN patients (p=0.035). Serum Spexin levels were negatively correlated with neuropathic pain score. Compared with individuals with higher levels of Spexin, the prevalence rate of painful DPN in those with lower levels of Spexin was significantly higher. Binary logistic regression analysis showed that the odds ratios for painful DPN were significantly elevated along with decreasing Spexin levels even after adjusting for age, sex, BMI, diabetes duration, HbA1c, 2hPBG, hypertension and smoking or drinking status. serum Spexin levels have a sensitivity of 84.1% and a specificity of 56.2% for predicting painful DPN.Conclusions: Decreased serum Spexin levels were strongly associated with painful DPN, suggesting a possible role of this peptide in pain-related pathogenesis.


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