Possible mechanism of protective effect of thalidomide in STZ-induced-neuropathic pain behavior in rats

Taliyan, Rajeev; Sharma, Pankaj

doi:10.1007/s10787-011-0106-4

Cited by 31 publications

(17 citation statements)

References 38 publications

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“…While previous studies have shown 18 that systemic administrations of thalidomide can strongly prevent the mechanical allodynia and thermal hyperalgesia in streptozotocin (STZ)-induced type 1 diabetic neuropathy (Chauhan et al, 2012;Huang et al, 2014;Taliyan and Sharma 2012), our study first demonstrated that supraspinal mechanisms of thalidomide play a critical role in modulations of type 2 diabetes induced neuropathic pain. Our results further suggested that TNFα and IL-1β mediated NFκB signaling in the RVM may contribute to the modulations of type 2 diabetes induced neuropathic pain.…”

Section: Discussionmentioning

confidence: 57%

“…Furthermore, recent studies have shown that thalidomide can strongly prevent the mechanical allodynia and 5 thermal hyperalgesia in streptozotocin (STZ)-induced type 1 diabetic neuropathy (Chauhan et al, 2012;Huang et al, 2014;Taliyan and Sharma 2012). It has been reported that thalidomide can reduce the synthesis of TNFα and other pro-inflammatory cytokines including IL-1β (Sampaio et al, 1991;Singhal and Mehta 2002).…”

Section: Introductionmentioning

confidence: 99%

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Administrations of thalidomide into the rostral ventromedial medulla alleviates painful diabetic neuropathy in Zucker diabetic fatty rats

Yang

Zhang

Guan

et al. 2016

Brain Research Bulletin

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Section: Discussionmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Administrations of thalidomide into the rostral ventromedial medulla alleviates painful diabetic neuropathy in Zucker diabetic fatty rats

Yang

Zhang

Guan

et al. 2016

Brain Research Bulletin

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“…Hyperglycemia may mediate its damaging effects through excess generation of AGEs,[28] ROS and NO,[30] angiotension-II formation with deactivation of NO,[31] myocardial collagen deposition and fibrosis,[32] activation of DAG/PKC signal transduction pathway leads to reduction in tissue blood flow, increased vascular permeability, alterations in neovascularization and enhanced extracellular matrix deposition. [33] An increase in mitochondrial ROS generation, decreases NO levels, leads to myocardial inflammation and endothelial dysfunction via PARP [poly (ADP-ribose) polymerase], inhibition of which has been shown to reverse diabetic endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Protective effect and mechanism of Ginkgo biloba extract-EGb 761 on STZ-induced diabetic cardiomyopathy in rats

Saini¹,

Taliyan²,

Sharma³

2014

Phcog Mag

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Diabetes mellitus (DM) is a complex metabolic disorder which leads to development of various long-term complications including cardiomyopathy. Oxidative stress due to hyperglycemia plays a key role in the development and progression of diabetic cardiomyopathy (DC). Oxidative stress causes the opening of mitochondrial permeability transition pore (mPTP) eventually leading to myocardium dysfunction. The Ginkgo biloba extract (EGb 761) has antioxidant and mitochondrial membrane potential stabilizing property. Therefore, this study was designed to evaluate the effect of EGb 761 and its possible mechanism of action in DC.Materials and Methods:DM was induced by single injection of Streptozotocin (STZ) (50 mg/kg, i.p.) and cardiac dysfunction was developed on 8th weeks after STZ injection. Cardiac dysfunction was assessed by measuring left ventricle weight/body weight (LVW/BW) ratio, left ventricle (LV) collagen content, LV protein content, serum lactate dehydrogenase (LDH) level.Results:EGb 761 treatment (started after 7th week of STZ injection and continued for 3 weeks) attenuated cardiac dysfunction in diabetic rats as evidenced by a decrease in LV collagen content, protein content, LVW/BW ratio, serum LDH level. Moreover, EGb 761 attenuated the oxido-nitrosative stress (thiobarbituric acid reactive substances, superoxide anion generation, myocardium nitrite) and concomitantly improved the antioxidant enzyme (reduced glutathione) level as compared to untreated diabetic rats. However, protective effect of EGb 761 was inhibited by atractyloside (mPTP opener) that was given for 3 weeks, 30 min before the EGb 761 treatment. These results indicate that EGb 761 corrects diabetic cardiac dysfunction probably by its direct radical scavenging activity and its ability to inhibit the opening of mPTP channel since the cardioprotective effect of EGb 761 was completely abolished by atractyloside.

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“…Importantly, recent research has shown that thalidomide treatment can reduce thermal hyperalgesia and allodynia in an animal model of neuropathic pain (Cata, Weng, & Dougherty, ), and strongly attenuate the mechanical allodynia in an animal model of type 1 diabetic neuropathy (Chauhan, Taliyan, & Sharma, ; Huang et al, ; Taliyan & Sharma, ). These effects likely involve the RVM, since intra‐RVM thalidomide treatment was able to dose‐dependently decrease mechanical allodynia in diabetic rats (Yang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Administrations of thalidomide into the rostral ventromedial medulla produce antinociceptive effects in a rat model of postoperative pain

Song

et al. 2017

J of Neuroscience Research

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The rostral ventromedial medulla (RVM) is highly involved in pain signal transmissions. Previous studies have shown that thalidomide is anti-nociceptive. Thus, we evaluated the neurobiological mechanisms of thalidomide in the RVM in the regulation of postoperative pain. We used a rat model of postoperative pain to investigate the effects of intra-RVM thalidomide treatments on postoperative pain, and evaluate the role of cannabinoid receptors in the effects of intra-RVM thalidomide treatments on GABAergic neurotransmission in the RVM neurons. We found intra-RVM thalidomide treatments reduced incisional surgery induced mechanical allodynia. This phenomenon was associated with attenuation of the frequency and amplitude of miniature inhibitory postsynaptic currents (mIPSCs) and spontaneous IPSCs (sIPSCs) in RVM neurons. Furthermore, applications of WIN 55,212-3 mesylate, a non-selective cannabinoid receptor antagonist reversed the effects of repeated thalidomide treatment on the frequency but not the amplitude of mIPSCs and sIPSCs. Finally, we found that repeated thalidomide treatment robustly enhanced CB2 receptor expression, but slightly reduced CB1 receptor expression, in the RVM. These results suggested that the antinociceptive effects of thalidomide in the RVM likely involve the attenuation of GABA release, which are critically regulated by cannabinoid receptors.

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Possible mechanism of protective effect of thalidomide in STZ-induced-neuropathic pain behavior in rats

Abstract: It may be concluded that thalidomide has a beneficial effect in neuropathic pain by decreasing cytokines (TNF-α) and nitric oxide level and may provide a novel promising therapeutic approach for managing painful diabetic neuropathy.

Cited by 31 publications

References 38 publications

Administrations of thalidomide into the rostral ventromedial medulla alleviates painful diabetic neuropathy in Zucker diabetic fatty rats

Administrations of thalidomide into the rostral ventromedial medulla alleviates painful diabetic neuropathy in Zucker diabetic fatty rats

Protective effect and mechanism of Ginkgo biloba extract-EGb 761 on STZ-induced diabetic cardiomyopathy in rats

Administrations of thalidomide into the rostral ventromedial medulla produce antinociceptive effects in a rat model of postoperative pain

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