scholarly journals Antiallodynic and anti-inflammatory effects of intrathecal R-PIA in a rat model of vincristine-induced peripheral neuropathy

2020 ◽  
Vol 73 (5) ◽  
pp. 434-444 ◽  
Author(s):  
Kyungmi Kim ◽  
Wonyeong Jeong ◽  
In Gu Jun ◽  
Jong Yeon Park
Keyword(s):  
Peripheral Neuropathy ◽  
Rat Model ◽  
Thermal Hyperalgesia ◽  
Mechanical Hyperalgesia ◽  
Cold Allodynia ◽  
Adenosine A1 Receptors ◽  
Tnf Α ◽  
Adenosine A1 ◽  
Α Level ◽  
Antiallodynic Effect

Background: Studies investigating the correlation between spinal adenosine A1 receptors and vincristine-induced peripheral neuropathy (VIPN) are limited. This study explored the role of intrathecal N6-(2-phenylisopropyl)-adenosine R-(-)isomer (R-PIA) in the rat model of VIPN. Methods: Vincristine (100 μg/kg) was intraperitoneally administered for 10 days (two 5-day cycles with a 2-day pause) and VIPN was induced in rats. Pain was assessed by evaluating mechanical hyperalgesia, mechanical dynamic allodynia, thermal hyperalgesia, cold allodynia, and mechanical static allodynia. Biochemically, tumor necrosis factor-alpha (TNF-α) level and myeloperoxidase (MPO) activity were measured in the tissue from beneath the sciatic nerve.Results: Vincristine administration resulted in the development of cold allodynia, mechanical hyperalgesia, thermal hyperalgesia, mechanical dynamic allodynia, and mechanical static allodynia. Intrathecally administered R-PIA (1.0 and 3.0 μg/10 μl) reversed vincristine-induced neuropathic pain (cold and mechanical static allodynia). The attenuating effect peaked 15 min after intrathecal administration of R-PIA after which it decreased until 180 min. However, pretreatment with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 μg/10 μl) 15 min before intrathecal R-PIA administration significantly attenuated the antiallodynic effect of R-PIA. This antiallodynic effect of intrathecal R-PIA may be mediated through adenosine A1 receptors in the spinal cord. Intrathecally administered R-PIA also attenuated vincristine-induced increases in TNF-α level and MPO activity. However, pretreatment with intrathecal DPCPX significantly reversed this attenuation.Conclusions: These results suggest that intrathecally administered R-PIA attenuates cold and mechanical static allodynia in a rat model of VIPN, partially due to its anti-inflammatory actions.

Effect of flavonol and its dimethoxy derivatives on paclitaxel-induced peripheral neuropathy in mice

2018 ◽  
Vol 29 (5) ◽  
pp. 525-535 ◽  
Author(s):  
Vijaykumar Sayeli ◽  
Jagan Nadipelly ◽  
Parimala Kadhirvelu ◽  
Binoy Varghese Cheriyan ◽  
Jaikumar Shanmugasundaram ◽  
...  
Keyword(s):  
Free Radicals ◽  
Peripheral Neuropathy ◽  
Proinflammatory Cytokines ◽  
Interleukin 1 ◽  
Thermal Hyperalgesia ◽  
Hot Water ◽  
Tactile Allodynia ◽  
Dependent Manner ◽  
Cold Allodynia ◽  
Tnf Α

AbstractBackground:Peripheral neuropathy is the dose limiting side effect of many anticancer drugs. Flavonoids exhibit good antinociceptive effect in animal models. Their efficacy against different types of nociception has been documented. The present study investigated the effect of flavonol (3-hydroxy flavone), 3′,4′-dimethoxy flavonol, 6,3′-dimethoxy flavonol, 7,2′-dimethoxy flavonol and 7,3′-dimethoxy flavonol against paclitaxel-induced peripheral neuropathy in mice.Methods:A single dose of paclitaxel (10 mg/kg, i.p.) was administered to induce peripheral neuropathy in mice and the manifestations of peripheral neuropathy such as tactile allodynia, cold allodynia and thermal hyperalgesia were assessed 24 h later by employing Von Frey hair aesthesiometer test, acetone bubble test and hot water tail immersion test, respectively. The test compounds were prepared as a suspension in 0.5% carboxymethyl cellulose and were administered s.c. in various doses (25, 50, 100 and 200 mg/kg). The above behavioral responses were assessed prior to and 30 min after drug treatment. In addition, the effect of test compounds on proinflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1β) and free radicals was investigated by using suitablein vitroassays.Results:A dose-dependent attenuation of tactile allodynia, cold allodynia and thermal hyperalgesia was evidenced in mice treated with flavonol derivatives. The test compounds inhibited TNF-α, IL-1β and free radicals in a concentration-dependent manner.Conclusions:These results revealed that flavonol and its dimethoxy derivatives ameliorated the manifestations of paclitaxel-induced peripheral neuropathy in mice. The inhibition of proinflammatory cytokines and free radicals could contribute to this beneficial effect.

The Effect of Electroconvulsive Treatment on Thermal Hyperalgesia and Mechanical Allodynia in a Rat Model of Peripheral Neuropathy

1998 ◽  
Vol 86 (3) ◽  
pp. 584-587 ◽  
Author(s):  
Masahiko Shibata ◽  
Satoshi Wakisaka ◽  
Takaya Inoue ◽  
Tadao Shimizu ◽  
Ikuto Yoshiya
Keyword(s):  
Peripheral Neuropathy ◽  
Rat Model ◽  
Mechanical Allodynia ◽  
Thermal Hyperalgesia ◽  
Electroconvulsive Treatment

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

201 HCN Channels Blockade Attenuates Chemotherapy-Induced Pain

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 254-254
Author(s):  
Kun Hu ◽  
Zerong You ◽  
Weihua Ding ◽  
Jianren Mao
Keyword(s):  
Peripheral Neuropathy ◽  
Rat Model ◽  
Dorsal Root ◽  
Mechanical Hyperalgesia ◽  
Hcn Channels ◽  
Oxaliplatin Treatment ◽  
Gene Transcripts ◽  
Pre Treatment ◽  
Chemotherapy Agents ◽  
Therapeutic Avenue

Abstract INTRODUCTION Painful peripheral neuropathy is a common dose-limiting side effect caused by chemotherapy agents, such as oxaliplatin. Mechanisms underlying this devastating condition are largely unknown. METHODS We established a rat model of chemotherapy induced pain by administering oxaliplatin at 2 mg/Kg for 5 consecutive days. Mechanical hyperalgesia, a typical nociceptive pain behavior, developed after treatment with oxaliplatin. We investigated the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in the dorsal root ganglia (DRG) at both gene transcripts level (real-time PCR) and protein level (immunofluorescence). In addition, we examined the functional significance of HCN upregulation after oxaliplatin treatment by using a pan HCN channels blocker-ZD 7288. RESULTS >DRG HCN 1 and HCN 2 were higher in oxaliplatin- treated rats than saline-treated controls, both for gene transcripts and proteins. ZD7288, when administered intrathecally, was able to alleviate, albeit not abrogate, oxaliplatin induced-pain. Interestingly, pre-treatment with ZD7288 prior to oxaliplatin administration did not prevent the development of mechanical hyperalgesia. CONCLUSION Taken together, HCN1 and HCN2 channels are upregulated by oxaliplatin treatment, and that HCN blockade alleviates oxaliplatin-induced pain. Therefore, targeting HCN channels may provide a therapeutic avenue to treat chemotherapy induced-pain.

Pre-injury lidocaine treatment prevents thermal hyperalgesia and cutaneous thermal abnormalities in a rat model of peripheral neuropathy

Pain ◽  
1995 ◽  
Vol 61 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Maria Luisa Sotgiu ◽  
Anna Castagna ◽  
Marco Lacerenza ◽  
Paolo Marchettini
Keyword(s):  
Peripheral Neuropathy ◽  
Rat Model ◽  
Thermal Hyperalgesia

A hydro-ethanolic extract of Synedrella nodiflora (L.) Gaertn ameliorates hyperalgesia and allodynia in vincristine-induced neuropathic pain in rats

2015 ◽  
Vol 26 (4) ◽  
Author(s):  
Patrick Amoateng ◽  
Samuel Adjei ◽  
Dorcas Osei-Safo ◽  
Elvis Ofori Ameyaw ◽  
Believe Ahedor ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cold Water ◽  
Thermal Hyperalgesia ◽  
Ethanolic Extract ◽  
Mechanical Hyperalgesia ◽  
Sprague Dawley ◽  
Cold Allodynia ◽  
Sprague Dawley Rats ◽  
Vincristine Sulphate ◽  
Synedrella Nodiflora

Abstract: The hydro-ethanolic extract of: Neuropathic pain was induced in Sprague-Dawley rats by injecting 100 μg/kg of vincristine sulphate on alternative days for 6 days (days 0, 2, 4, 8, 10 and 12). Vincristine-induced cold allodynia, mechanical hyperalgesia and thermal hyperalgesia were measured pre-vincristine administration and on days 15, 17 and 19 post-vincristine administration. The rats were then treated withSNE and pregabalin produced analgesic properties observed as increased paw withdrawal latencies to mechanical, tactile, cold water stimuli and thermal hyperalgesic tests during the 5 days of treatment.: The findings suggest that hydro-ethanolic extract of

The Effect of Electroconvulsive Treatment on Thermal Hyperalgesia and Mechanical Allodynia in a Rat Model of Peripheral Neuropathy

1998 ◽  
Vol 86 (3) ◽  
pp. 584-587 ◽  
Author(s):  
Masahiko Shibata ◽  
Satoshi Wakisaka ◽  
Takaya Inoue ◽  
Tadao Shimizu ◽  
Ikuto Yoshiya
Keyword(s):  
Peripheral Neuropathy ◽  
Rat Model ◽  
Mechanical Allodynia ◽  
Thermal Hyperalgesia ◽  
Electroconvulsive Treatment
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