The effect of thioctic acid on allodynia in a rat vincristine-induced neuropathy model

Kahng, Jimin; Kim, Tae Kwan; Chung, Eun Yong; Kim, Yeo Ju; Moon, Jeong Yeon

doi:10.1177/0300060515569287

Cited by 11 publications

(9 citation statements)

References 30 publications

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“…All these data suggested a prominently active role of the dextrorotatory enantiomer in the racemic mixture. Accordingly, previous studies on chemotherapyinduced neuropathy described similar results: thioctic acid acutely dosed to vincristine-treated rats reversed allodynia symptoms; chronic injections of 15, 30, and 60 mg/kg of (+/−)-thioctic acid on neuropathic rodents, which were given paclitaxel, significantly reduced mechanical and cold allodynia (Kahng et al, 2015;Sun et al, 2019). As previously reported (Tomassoni et al, 2013), SHR rats showed higher values of systolic blood pressure as compared to WKY rats.…”

Section: Discussionsupporting

confidence: 80%

Comparative Assessment of the Activity of Racemic and Dextrorotatory Forms of Thioctic (Alpha-Lipoic) Acid in Low Back Pain: Preclinical Results and Clinical Evidences From an Open Randomized Trial

et al. 2021

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Peripheral neuropathies, characterized by altered nociceptive and muscular functions, are related to oxidative stress. Thioctic acid is a natural antioxidant existing as two optical isomers, but most clinically used as racemic mixture. The present study investigated the central nervous system’s changes which followed loose-ligation-derived compression of sciatic nerve, the putative neuroprotective role of thioctic acid and the pain-alleviating effect on low-back pain suffering patients. Loose ligation of the right sciatic nerve was performed in spontaneously hypertensive rats (SHR), a model of increased oxidative stress, and in normotensive Wistar-Kyoto rats (WKY). Animals with sciatic nerve ligation were left untreated or were treated intraperitoneally for 15 days with 250 μmol·kg−1·die−1 of (+/−)-thioctic acid; 125 μmol·kg−1·die−1 of (+/−)-thioctic acid; 125 μmol·kg−1·die−1 of (+)-thioctic acid lysine salt; 125 μmol·kg−1·die−1 of (−)-thioctic acid; 300 μmol·kg−1·die−1 pregabalin. Control SHR and WKY rats received the same amounts of vehicle. The clinical trial NESTIORADE (Sensory-Motor Neuropathies of the Sciatic Nerve: Comparative evaluation of the effect of racemic and dextro-rotatory forms of thioctic acid) examined 100 patients (49 males and 51 females aged 53 ± 11 years) dividing them into two equal-numbered groups, each treated daily for 60 days with 600 mg of (+/−)-thioctic acid or (+)-thioctic acid, respectively. The trial was registered prior to patient enrollment at EudraCT website (OSSC Number: 2011-000964-81). In the preclinical study, (+)-thioctic acid was more active than (+/−)- or (−)-enantiomers in relieving pain and protecting peripheral nerve as well as in reducing oxidative stress and astrogliosis in the spinal cord. Main findings of NESTIORADE clinical trial showed a greater influence on painful symptomatology, a quicker recovery and a better impact on quality of life of (+)-thioctic acid vs. (+/−)-thioctic acid. These data may have a pharmacological and pharmacoeconomical relevance and suggest that thioctic acid, above all (+)-enantiomer, could be considered for treatment of low-back pain involving neuropathy.

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Section: Discussionsupporting

confidence: 80%

Comparative Assessment of the Activity of Racemic and Dextrorotatory Forms of Thioctic (Alpha-Lipoic) Acid in Low Back Pain: Preclinical Results and Clinical Evidences From an Open Randomized Trial

et al. 2021

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“…To confirm the establishment of the vincristine-induced pain model, the 50% PWT and PWL to the radiant heat stimulation were measured prior to vincristine administration and on days 1, 3, 7, 10, 14, and 21 post-administration. Consistent with previous reports ( 17 , 20 ), the results demonstrated that rats in the vincristine-treated group exhibited significant mechanical allodynia and thermal hyperalgesia ( Fig. 1 ).…”

Section: Resultssupporting

confidence: 92%

“…All animal experimental procedures were conducted in accordance with the guidelines of the International Association for the Study of Pain ( 20 ) and were approved by the Animal Experimentation Ethics Committee (AEEC) of Henan University (Kaifeng, China). Vincristine was used to induce neuropathy as previously described ( 20 ). Briefly, 75 µg/kg of vincristine sulfate (Hospira, Lake Forest, IL, USA) was administered once daily intraperitoneally (i.p.)…”

Section: Methodsmentioning

confidence: 99%

Sensitization of TRPV1 receptors by TNF‑α orchestrates the development of vincristine‑induced pain

Wang

Feng

et al. 2018

Oncol Lett

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Vincristine is one of the most common anticancer drugs clinically employed in the treatment of various malignancies. A major side effect associated with vincristine is the development of neuropathic pain, which is not readily relieved by available analgesics. Although efforts have been made to identify the pathogenesis of vincristine-induced neuropathic pain, the mechanisms underlying its pathogenesis have not been fully elucidated. In the present study, a neuropathic pain model was established in Sprague-Dawley rats by intraperitoneal injection of vincristine sulfate. The results demonstrated that vincristine administration induced the upregulation of transient receptor potential cation channel subfamily V member 1 (TRPV1) protein expression and current density in dorsal root ganglion (DRG) nociceptive neurons. Consistently, inhibition of TRPV1 with capsazepine alleviated vincristine-induced mechanical allodynia and thermal hyperalgesia in rats. Furthermore, vincristine administration induced the upregulation of tumor necrosis factor (TNF)-α production in DRGs, and inhibition of TNF-α synthesis with thalidomide in vivo reversed TRPV1 protein expression, as well as pain hypersensitivity induced by vincristine in rats. The present results suggested that TNF-α could sensitize TRPV1 by promoting its expression, thus leading to mechanical allodynia and thermal hyperalgesia in vincristine-treated rats. Taken together, these findings may enhance our understanding of the pathophysiological mechanisms underlying vincristine-induced pain.

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“…Vincristine sulphate was used to induce neuropathy as described by Kahng 26 with a little modification. VCR was dissolved in its solvent ampoule, which contained 10 ml sodium solution 0.9% and benzyl alcohol 0.9% with the dosage calculated on daily body‐weight at the dose of 0.1 mg/kg, every other day, in course of the study for 14 days.…”

Section: Methodsmentioning

confidence: 99%

The protective effect of modafinil on vincristine‐induced peripheral neuropathy in rats: A possible role for TRPA1 receptors

amirkhanloo

Karimi

Yousefi‐Manesh

et al. 2020

Basic Clin Pharma Tox

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The chemotherapy-induced peripheral neuropathy (CIPN) is a very common chemotherapy drawback. 1 Several reports indicated that vinca alkaloids, taxine, cisplatinum and many other chemotherapeutic drugs can lead to hyperpathia or hypersensitivity and induce neuropathic pain. Vincristine (VCR), a vinca alkaloid, is used as an anticancer agent for leukaemia and lymphoma. 2 Meanwhile, CIPN can limit VCR efficiency and reduce the cure rate. 3

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The effect of thioctic acid on allodynia in a rat vincristine-induced neuropathy model

Cited by 11 publications

References 30 publications

Comparative Assessment of the Activity of Racemic and Dextrorotatory Forms of Thioctic (Alpha-Lipoic) Acid in Low Back Pain: Preclinical Results and Clinical Evidences From an Open Randomized Trial

Comparative Assessment of the Activity of Racemic and Dextrorotatory Forms of Thioctic (Alpha-Lipoic) Acid in Low Back Pain: Preclinical Results and Clinical Evidences From an Open Randomized Trial

Sensitization of TRPV1 receptors by TNF‑α orchestrates the development of vincristine‑induced pain

The protective effect of modafinil on vincristine‐induced peripheral neuropathy in rats: A possible role for TRPA1 receptors

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