Protective Effects of Curcumin Against Paclitaxel-Induced Spinal Cord and Sciatic Nerve Injuries in Rats

Maier

2021

IJMS

Lesion or disease of the somatosensory system leads to the development of neuropathic pain. Peripheral neuropathic pain encompasses damage or injury of the peripheral nervous system. On the other hand, 10–15% of individuals suffer from acute postoperative pain followed by persistent pain after undergoing surgeries. Antidepressants, anticonvulsants, baclofen, and clonidine are used to treat peripheral neuropathy, whereas opioids are used to treat postoperative pain. The negative effects associated with these drugs emphasize the search for alternative therapeutics with better efficacy and fewer side effects. Curcumin, a polyphenol isolated from the roots of Curcuma longa, possesses antibacterial, antioxidant, and anti-inflammatory properties. Furthermore, the low bioavailability and fast metabolism of curcumin have led to the advent of various curcumin formulations. The present review provides a comprehensive analysis on the effects of curcumin and its formulations in preclinical and clinical studies of neuropathic and postoperative pain. Based on the positive outcomes from both preclinical and clinical studies, curcumin holds the promise of mitigating or preventing neuropathic and postoperative pain conditions. However, more clinical studies with improved curcumin formulations are required to involve its use as adjuvant to neuropathic and postoperative drugs.

Section: Curcumin and Neuropathic Pain—preclinical Studiesmentioning

confidence: 99%

Effects of Curcumin and Its Different Formulations in Preclinical and Clinical Studies of Peripheral Neuropathic and Postoperative Pain: A Comprehensive Review

Maier

2021

IJMS

Int J Life Sci Pharm Res

“…It has been reported that paclitaxel treatment induces mRNA expression of pro-inflammatory cytokines such as IL-1 β, IL-20, TNF-α, immune cell markers and increased levels of phosphorylated NF-κB in sciatic nerve, and lumbar DRG and spinal cord. 11,[28][29][30] Further, monocyte chemoattractant protein 1 (MCP-1) and circulating cytokines impairs the blood spinal cord permeability and triggers the influx of inflammatory mediators into spinal cord leading to activation of spinal immune cells. 10,29,[32][33][34] Moreover, repeated administration of paclitaxel has been found to activate nonneuronal immune cells, microglia and astrocytes, and CCchemokine ligand 3 (CCL3), IL-1β, IL-20, and TNF-α release in DRGs and spinal cord.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Ameliorates Paclitaxel-Induced Pain Hypersensitivity via Alleviation of Inflammation and Oxidative Stress in Rats

Pasupulati¹,

Satyanarayana²,

Bharathi³

et al. 2021

Painful peripheral neuropathy is the main dose-limiting and long lasting side-effect of paclitaxel therapy. Despite enormous research, there is no effective treatment for paclitaxel-induced peripheral neuropathic pain owing to poor understanding of pathophysiological mechanisms. Growing evidence indicates oxidative-nitrosative stress is one of the leading factors causing chemotherapy induced peripheral neuropathy. Recently, involvement of neuroinflammation has been suggested in the development of paclitaxel-induced neuropathic pain. It is postulated that abrogating cytokine release and improving antioxidant defenses might be suitable targets in controlling neuroinflammation and oxidative-nitrosative stress mediated nociceptive hypersensitivities. Therefore, the study evaluated the effect of curcumin on paclitaxel-induced neuropathic pain in rats. Peripheral neuropathy was induced by administration of paclitaxel (2 mg/kg per injection) intraperitoneally on four alternate days (days 0, 2, 4, 6). Thermal hyperalgesia and mechanical allodynia were assessed and the markers of inflammation and oxidative-nitrosative stress were estimated. Administration of curcumin (50 and 100 mg/kg, p.o.) for 2 weeks started 14 days after paclitaxel injection significantly alleviated paclitaxel-induced nociceptive behavioural hypersensitivity observed as reduced thermal hyperalgesia and mechanical allodynia. These observed ameliorative effects of curcumin on paclitaxel-induced neuropathic pain are accompanied by reduction of tumour necrosis factor-α, a pro-inflammatory cytokine, in both spinal cord and dorsal root ganglia and oxidative-nitrosative stress in spinal cord. The results of the present study demonstrated antihyperalgesic and antiallodynic effects of curcumin. Additional clinical studies are warranted to evaluate therapeutic potential of curcumin as antinociceptive agent in the treatment of paclitaxel-induced neuropathic pain.

Türk Doğa Ve Fen Dergisi

“…MDA, çoklu doymamış yağ asitlerinin oksidasyon ürünüdür ve artan MDA içeriği, lipid peroksidasyonunun önemli bir göstergesi olarak kabul edilmektedir [37][38][39]. Önceki çalışmalarda çeşitli toksik ajanların ROS üretimine bağlı olarak lipid peroksidayonu meydana getirdiğini ve buna bağlı olarak MDA seviyelerinde artışların olduğu bildirilmiştir [40][41][42][43][44]. Artan MDA seviyelerinin oksidatif stresin önemli bir göstergesi olduğunu ve oksidatif stresin de kalp dahil çeşitli dokularda toksisiteye yol açtığı yapılan çalışmalarda kanıtlanmıştır [28,[45][46][47] [15].…”

Section: Discussionunclassified

Bortezomib ile Kalp Hasarı Oluşturulan Ratlarda Berberinin Oksidatif ve Nitrozatif Stres Üzerine Etkisi

Gür

Kandemir²,

Genç³

2020

Öz: Bortezomib (BTZ), proteazom sistemini bloke ederek hücresel protein yıkımını engelleyen yeni nesil bir antineoplastik ilaçtır. Bu çalışmada BTZ kaynaklı kalp hasarına karşı bir izokinolin alkaloid olan berberinin (BBR) koruyucu etkileri araştırılmıştır. Çalışmada erkek Sprague Dawley cinsi ratlara 1., 3., 5. ve 7. günlerde periton içi 0,2 mg kg -1 BTZ ve 10 gün boyunca her gün 50 ve 100 mg kg -1 dozlarda BBR verildi. Ratların kalp dokularında malondialdehit (MDA), glutatyon (GSH), total antioksidan kapasite (TAK), total oksidan kapasite (TOK) ve nitrik oksit (NO) seviyeleri ile süperoksit dismutaz (SOD), katalaz (KAT), glutatyon peroksidaz (GPx) ve laktat dehidrogenaz (LDH) aktiviteleri biyokimyasal yöntemler ile analiz edildi. Veriler BTZ'nin kalp dokusunda MDA, NO ve TOK seviyelerini, serumda LDH aktivelerini ve oksidatif stres indeksini (OSI) önemli ölçüde arttırdığını, GSH ve TAK seviyeleri ile SOD, KAT ve GPx aktivitelerini azaltarak oksidatif stresi tetiklediğini buna bağlı olarak dokuda hasar oluşturduğunu gösterdi. Buna karşın BBR, BTZ'nin neden olduğu oksidatif stresi ve nitrozatif stresi hafifleterek kalp hasarına karşı koruyucu etki gösterdi. Sonuçlara göre BBR'nin, BTZ ile indüklenen kardiyak toksisiteye karşı daha ileri çalışmalardan sonra koruyucu olarak kullanılabileceğini gösterdi.