Neuroprotective effects of acetyl‐<scp>L</scp>‐carnitine on neuropathic pain and apoptosis: A role for the nicotinic receptor

Mannelli, Lorenzo Di Cesare; Ghelardini, Carla; Calvani, Menotti; Nicolai, Raffaella; Mosconi, Luigi; Toscano, Anna; Pacini, Alessandra; Bartolini, Alessandro

doi:10.1002/jnr.21815

Cited by 46 publications

(34 citation statements)

References 39 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, they decrease the toxic effects of free fatty acids by facilitating ␤ -oxidation [45] . Furthermore, strong inhibition of apoptosis and mitochondrial membrane permeability by carnitine and its ester derivatives has been reported by some studies [22,27,45,49,51] . In this study, the powerful antiapoptotic properties of AL-CAR might have an additional protective effect on cisplatin-treated kidneys.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Nephrotoxicity

Tüfekçi¹,

Güneş²,

Özoğul³

et al. 2009

Chemotherapy

View full text Add to dashboard Cite

Background/Aims: To evaluate the protective effects of acetyl L-carnitine (ALCAR) on cisplatin-induced nephrotoxicity in rats, and to gain insights into the possible protective mechanisms of ALCAR against nephrotoxicity. Methods: Twenty-eight Wistar rats were divided into four groups. Group 1 was administered saline only, group 2 was administered ALCAR, group 3 was administered cisplatin, and group 4 was administered ALCAR prior to cisplatin. Rats were sacrificed after 72 h of cisplatin/saline infusion. Serum creatinine and glomerular filtration rate values were obtained, and kidney samples were examined by light and electron microscopy. Apoptotic cell death and caspase-3, 8 and 9 activities were studied immunohistochemically. Results: In group 4, ALCAR administration resulted in an improvement in kidney function tests. Histopathological findings confirmed the biochemical data. Whilst the fusion of the foot processes of podocytes was observed in group 3, they were intact in group 4 on electron-microscopic examination. Apoptotic cell death and caspase-3, 8 and 9 activities were also decreased in group 4 compared to group 3. Conclusions: Antioxidative, antiapoptotic and anti-inflammatory properties of ALCAR were supported by the findings that this agent improves kidney function tests and has the effects of tissue protection and inhibition of apoptosis in cisplatin-induced nephrotoxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Nephrotoxicity

Tüfekçi¹,

Güneş²,

Özoğul³

et al. 2009

Chemotherapy

View full text Add to dashboard Cite

show abstract

“…Nicotinic acetylcholine receptors (nAChRs) have been suggested as potentially important signaling molecules in pain and neuroprotection [7,5,14,18,50]. nAChRs are pentameric ligand-gated ion channels composed of combinations of α and/or β subunits (α1–α10; β1–β4) [1].…”

Section: Introductionmentioning

confidence: 99%

α-Conotoxin RgIA protects against the development of nerve injury-induced chronic pain and prevents both neuronal and glial derangement

Mannelli

Cinci

Micheli

et al. 2014

Pain

Self Cite

105

View full text Add to dashboard Cite

Neuropathic pain affects millions of people worldwide causing substantial disability and greatly impairing quality of life. Commonly used analgesics or anti-hyperalgesic compounds are generally characterized by limited therapeutic outcomes. Thus, there is a compelling need for novel therapeutic strategies able to prevent nervous tissue alterations responsible for chronic pain. The α9α10 nAChR antagonist α-conotoxin RgIA (RgIA), a peptide isolated from the venom of a carnivorous cone snail, induces relief in both acute and chronic pain models. To evaluate potential disease-modifying effects of RgIA, the compound was given to rats following chronic constriction injury (CCI) of the sciatic nerve. Two or 10 nmol RgIA injected intramuscularly once a day for 14 days reduced the painful response to suprathreshold stimulation, increased pain threshold to non-noxious stimuli, and normalized alterations in hind limb weight bearing. Histological analysis of the sciatic nerve revealed that RgIA prevented CCI-induced decreases of axonal compactness and diameter, loss of myelin sheath and decreases in the fiber number. Moreover, RgIA significantly reduced edema and inflammatory infiltrate, including a decrease of CD86+ macrophages. In L4–L5 dors the inflammatory infiltrate consistent with a disease-modifying effect. In the dorsal horn of the spinal cord, RgIA prevented CCI-induced activation of microglia and astrocytes. These data suggest that RgIA-like compounds may represent a novel class of therapeutics for neuropathic pain that protects peripheral nervous tissues as well as prevents central maladaptive plasticity by inhibiting glial cell activation.

show abstract

“…Several reports support a role for acetylcholine (ACh) in the inhibition and modulation of the transmission of nociceptive information [38, 39]. It has been demonstrated that the cholinergic system is involved in antinociceptive mechanisms, by (1) the activation of the GABAergic system [40]; (2) Muscarinic receptors (mAChR) mediation on spinal and (3) supraspinal sites [41, 42]; (4) inhibition enhancement of nicotinic receptors in the spinal dorsal horn [43]; (5) peripheral mAChR [44] or by interaction with the opioid system; however, this correlation is still not well elucidated.…”

Section: Discussionmentioning

confidence: 99%

Libidibia ferreaMature Seeds Promote Antinociceptive Effect by Peripheral and Central Pathway: Possible Involvement of Opioid and Cholinergic Receptors

Sawada

Monteiro

Rabelo

et al. 2014

BioMed Research International

View full text Add to dashboard Cite

Libidibia ferrea (LF) is a medicinal plant that holds many pharmacological properties. We evaluated the antinociceptive effect in the LF aqueous seed extract and Lipidic Portion of Libidibia ferrea (LPLF), partially elucidating their mechanisms. Histochemical tests and Gas chromatography of the LPLF were performed to characterize its fatty acids. Acetic acid-induced abdominal constriction, formalin-induced pain, and hot-plate test in mice were employed in the study. In all experiments, aqueous extract or LPLF was administered systemically at the doses of 1, 5, and 10 mg/kg. LF aqueous seed extract and LPLF demonstrated a dose-dependent antinociceptive effect in all tests indicating both peripheral anti-inflammatory and central analgesia properties. Also, the use of atropine (5 mg/kg), naloxone (5 mg/kg) in the abdominal writhing test was able to reverse the antinociceptive effect of the LPLF, indicating that at least one of LF lipids components is responsible for the dose related antinociceptive action in chemical and thermal models of nociception in mice. Together, the present results suggested that Libidibia ferrea induced antinociceptive activity is possibly related to its ability to inhibit opioid, cholinergic receptors, and cyclooxygenase-2 pathway, since its main component, linoleic acid, has been demonstrated to produce such effect in previous studies.

show abstract

Neuroprotective effects of acetyl‐L‐carnitine on neuropathic pain and apoptosis: A role for the nicotinic receptor

Cited by 46 publications

References 39 publications

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Nephrotoxicity

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Nephrotoxicity

α-Conotoxin RgIA protects against the development of nerve injury-induced chronic pain and prevents both neuronal and glial derangement

Libidibia ferreaMature Seeds Promote Antinociceptive Effect by Peripheral and Central Pathway: Possible Involvement of Opioid and Cholinergic Receptors

Contact Info

Product

Resources

About