Neuroprotective and antihyperalgesic effects of orexin-A in rats with painful diabetic neuropathy

Niknia, Seddigheh; Kaeidi, Ayat; Hajizadeh, Mohammad Reza; Mirzaei, Mohammad Reza; Khoshdel, Alireza; Hajializadeh, Zahra; Fahmidehkar, Mohammad Ali; Mahmoodi, Mehdi

doi:10.1016/j.npep.2018.11.001

Cited by 8 publications

(4 citation statements)

References 64 publications

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“…In the current study, the number of NeuN positive cells was found to decrease in the spinal cords of STZ rats suggesting a reduced neuronal number. This decrease may be at least in part due to neuronal apoptosis as demonstrated by increased caspase3 expression in the diabetic spinal cord group, similar to the results of Inam et al (2019), Niknia et al (2019), andMandour et al (2022).…”

Section: Discussionsupporting

confidence: 83%

Suppression of neuronal apoptosis and glial activation with modulation of Nrf2/HO-1 and NF-kB signaling by curcumin in streptozotocin-induced diabetic spinal cord central neuropathy

Elsayed

Rabei²,

Elshaer³

et al. 2023

Front. Neuroanat.

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IntroductionDiabetes is a global disease, commonly complicated by neuropathy. The spinal cord reacts to diabetes by neuronal apoptosis, microglial activation, and astrocytosis, with a disturbance in neuronal and glial Nuclear factor erythroid 2-related factor/Heme oxygenase-1 (Nrf2/HO-1) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling. Curcumin, a bioactive natural substance, showed neuroprotective role in many diseases. However, its role in the treatment of the diabetic central neuropathy of spinal cord and the underlying mechanisms still need clarification. The present study tried to evaluate the role of curcumin in diabetes-induced central neuropathy of the spinal cord in rats.MethodsTwenty rats were divided into three groups; group 1: a negative control group; group 2: received streptozotocin (STZ) to induce type I diabetes, and group 3: received STZ + Curcumin (150 mg/kg/day) for eight weeks. The spinal cords were examined for histopathological changes, and immunohistochemical staining for Glia fibrillary acidic protein (GFAP); an astrocyte marker, Ionized calcium-binding adaptor molecule 1 (Iba1), a microglial marker, neuronal nuclear protein (NeuN); a neuronal marker, caspase-3; an apoptosis marker, Nrf2/HO-1, NF-kB, and oxidative stress markers were assessed.ResultsCurcumin could improve spinal cord changes, suppress the expression of Iba1, GFAP, caspase-3, and NF-kB, and could increase the expression of NeuN and restore the Nrf2/HO-1 signaling.DiscussionCurcumin could suppress diabetic spinal cord central neuropathy, glial activation, and neuronal apoptosis with the regulation of Nrf2/HO-1 and NF-kB signaling.

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Section: Discussionsupporting

confidence: 83%

Suppression of neuronal apoptosis and glial activation with modulation of Nrf2/HO-1 and NF-kB signaling by curcumin in streptozotocin-induced diabetic spinal cord central neuropathy

Elsayed

Rabei²,

Elshaer³

et al. 2023

Front. Neuroanat.

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“…to find out any withdrawal behavior (n = 8); in Group 2, animals received subcutaneous administration of morphine (6,16,26,36,46, 56 and 66 mg/kg, 2 ml/kg) for 7 days and then naloxone (2.5 mg/kg, i.p.) was injected on day 8 to evaluate morphine withdrawal signs (n = 8); Group 3 and 4, morphine-treated rats receiving intra-PVT microinjection of orexin-A (100 μM, 200 nl, n = 8), or its vehicle (saline, 200 nl, n = 8) respectively during 7 days before each morphine injection [21] and then naloxone were administered 24 hrs after the last morphine administration.…”

Section: Animalsmentioning

confidence: 99%

Administration of Orexin-A into the Rat Thalamic Paraventricular Nucleus Enhances the Naloxone Induced Morphine Withdrawal

2022

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Objective Orexin neuropeptides are implicated in physical dependence on opioids and expression of withdrawal symptoms in drug abuse. The paraventricular nucleus of the midline thalamus (PVT) has a high expression of orexin receptors. The current research studied the effect of orexin-A in the PVT area on the development of behavioral indices produced by morphine withdrawal in rats. Methods Male Wistar rats weighing 250–300 gr were utilised. To produce drug dependence, morphine (6, 16, 26, 36, 46, 56, and 66 mg/kg, 2 ml/kg) was injected at an interval of 24 hrs for 7 days. To assess the involvement of the orexin in withdrawal syndrome, we injected orexin-A (100 μM, 200 nl) into the PVT for 7 days before each morphine injection. On the day after the last injection of morphine, naloxone (2.5 mg/kg, i.p.) was injected to elicit the morphine withdrawal symptoms which were observed and checked for 25 min. Results The results of the current research showed that the orexin-A in PVT enhances the severity of behavioral symptoms prompted by the injection of naloxone in drug-dependent rats. Conclusions These observations imply that targeting the orexin receptors in PVT might exhibit a new therapeutic strategy for the future treatment of dependence.

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“…Folic acidanother potential neuroprotective agent-increases the expression of nerve growth factor, leading to increased CMAP amplitudes and reduced peripheral nerve fibrosis [135]. At the same time, orexin-A demonstrated anti-hyperalgesic and neuroprotective effects in rats with diabetic peripheral neuropathy [136]. Much attention is also given to neuronal growth factors because endogenous growth factors boost neuronal health and survival [123].…”

Section: Neuroprotectionmentioning

confidence: 99%

Peripheral neuropathy: A neglected cause of disability in COPD – A narrative review

Odajiu¹,

Covanţev²,

Sivapalan³

et al. 2022

Respiratory Medicine

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Neuroprotective and antihyperalgesic effects of orexin-A in rats with painful diabetic neuropathy

Cited by 8 publications

References 64 publications

Suppression of neuronal apoptosis and glial activation with modulation of Nrf2/HO-1 and NF-kB signaling by curcumin in streptozotocin-induced diabetic spinal cord central neuropathy

Suppression of neuronal apoptosis and glial activation with modulation of Nrf2/HO-1 and NF-kB signaling by curcumin in streptozotocin-induced diabetic spinal cord central neuropathy

Administration of Orexin-A into the Rat Thalamic Paraventricular Nucleus Enhances the Naloxone Induced Morphine Withdrawal

Peripheral neuropathy: A neglected cause of disability in COPD – A narrative review

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