A curcumin derivative J147 ameliorates diabetic peripheral neuropathy in streptozotocin (STZ)-induced DPN rat models through negative regulation AMPK on TRPA1

Lv, Juan; Cao, Liu; Zhang, Rui; Bai, Feng‐Wu; Wei, Pengfei

doi:10.1590/s0102-865020180060000008

Cited by 18 publications

(20 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…New formulations of curcumin have also shown an antinociceptive effect on mechanical, cold, and thermal hypersensitivity in models of DPN with sometimes superior effects to unformulated curcumin. For example, Ly et al 2018, showed in male SPF rats that curcumin J147 (hybrid molecule between curcumin and cyclohexyl-bisphenol-A) decreased STZ-induced mechanical hypersensitivity in the von Frey test [ 50 ]. In addition, an alternative curcumin delivery system, self-nano-emulsifying drug delivery system (SNEDDS) curcumin, reversed, in male SD rat model of DPN, the mechanical hypersensitivity to hot and cold measured by von Frey test and tail flick hot and cold immersions, respectively [ 51 ].…”

Section: Curcumin Studies In Animal Models Of Pnmentioning

confidence: 99%

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

et al. 2020

View full text Add to dashboard Cite

Peripheral neuropathies (PN) can be triggered after metabolic diseases, traumatic peripheral nerve injury, genetic mutations, toxic substances, and/or inflammation. PN is a major clinical problem, affecting many patients and with few effective therapeutics. Recently, interest in natural dietary compounds, such as polyphenols, in human health has led to a great deal of research, especially in PN. Curcumin is a polyphenol extracted from the root of Curcuma longa. This molecule has long been used in Asian medicine for its anti-inflammatory, antibacterial, and antioxidant properties. However, like numerous polyphenols, curcumin has a very low bioavailability and a very fast metabolism. This review addresses multiple aspects of curcumin in PN, including bioavailability issues, new formulations, observations in animal behavioral tests, electrophysiological, histological, and molecular aspects, and clinical trials published to date. The, review covers in vitro and in vivo studies, with a special focus on the molecular mechanisms of curcumin (anti-inflammatory, antioxidant, anti-endoplasmic reticulum stress (anti-ER-stress), neuroprotection, and glial protection). This review provides for the first time an overview of curcumin in the treatment of PN. Finally, because PN are associated with numerous pathologies (e.g., cancers, diabetes, addiction, inflammatory disease...), this review is likely to interest a large audience.

show abstract

Section: Curcumin Studies In Animal Models Of Pnmentioning

confidence: 99%

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

et al. 2020

View full text Add to dashboard Cite

show abstract

“…5-HT 1B receptor is responsible for the dynamic accommodation of the serotonergic pathway that has been implicated in several functions such as cognition and emotion ( Blier and Ward, 2003 ; Manuel-Apolinar and Meneses, 2004 ). The antidepressant-like effects of curcumin have been proven to be related to 5-HT 1A and 5-HT 1B receptors ( Lv et al, 2018 ), as shown in our previous studies that suggested that curcumin reversed the decreases in 5-HT and 5-HT 1A receptor mRNA expression in chronically stressed rats ( Xu et al, 2005a , 2011a ). Pre-treatment with a NAD-299 or isamoltane (5-HT 1B receptor antagonist) abolished the neuroprotective effects of curcumin, indicating that 5-HT 1A and 5-HT 1B receptors may indeed mediate the effects of curcumin ( Xu et al, 2011a , b ).…”

Section: Discussionmentioning

confidence: 72%

“…5-HT 1A and 5-HT 1B receptors are responsible for pathological changes in depression ( Perera et al, 2001 ; Blier and Ward, 2003 ). 5-HT 1A receptor is one of 14 known 5-HT receptor variants that gets the most attention largely owing to its key role in the pathogenesis of depression and the action of antidepressants ( Lv et al, 2018 ). 5-HT 1B receptor is responsible for the dynamic accommodation of the serotonergic pathway that has been implicated in several functions such as cognition and emotion ( Blier and Ward, 2003 ; Manuel-Apolinar and Meneses, 2004 ).…”

Section: Discussionmentioning

confidence: 99%

“…Pre-treatment with a NAD-299 or isamoltane (5-HT 1B receptor antagonist) abolished the neuroprotective effects of curcumin, indicating that 5-HT 1A and 5-HT 1B receptors may indeed mediate the effects of curcumin ( Xu et al, 2011a , b ). J147, a curcumin derivative, has neuroprotective effects in Alzheimer’s disease and in streptozotocin-induced diabetic peripheral neuropathy ( Kulkarni et al, 2008 ; Lv et al, 2018 ). Acute treatment of J147 exerts antidepressant-like effects in mouse model of despair tests, mainly through serotonergic synaptic availability ( Kulkarni et al, 2008 ; Xu et al, 2011a ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Sub-Acute Treatment of Curcumin Derivative J147 Ameliorates Depression-Like Behavior Through 5-HT1A-Mediated cAMP Signaling

Chen

et al. 2020

Front. Neurosci.

View full text Add to dashboard Cite

Background Major depressive disorder (MDD) is a severe mental disorder related to the deficiency of monoamine neurotransmitters, particularly to abnormalities of 5-HT (5-hydroxytryptamine, serotonin) and its receptors. Our previous study suggested that acute treatment with a novel curcumin derivative J147 exhibited antidepressant-like effects by increasing brain derived neurotrophic factor (BDNF) level in the hippocampus of mice. The present study expanded upon our previous findings and investigated the antidepressant-like effects of sub-acute treatment of J147 for 3 days in male ICR mice and its possible relevancy to 5-HT 1A and 5-HT 1B receptors and downstream cAMP-BDNF signaling. Methods J147 at doses of 1, 3, and 9 mg/kg (via gavage) was administered for 3 days, and the anti-immobility time in the forced swimming and tail suspension tests (FST and TST) was recorded. The radioligand binding assay was used to determine the affinity of J147 to 5-HT 1A and 5-HT 1B receptor. Moreover, 5-HT 1A or 5-HT 1B agonist or its antagonist was used to determine which 5-HT receptor subtype is involved in the antidepressant-like effects of J147. The downstream signaling molecules such as cAMP, PKA, pCREB, and BDNF were also measured to determine the mechanism of action. Results The results demonstrated that sub-acute treatment of J147 remarkably decreased the immobility time in both the FST and TST in a dose-dependent manner. J147 displayed high affinity in vitro to 5-HT 1A receptor prepared from mice cortical tissue and was less potent at 5-HT 1B receptor. These effects of J147 were blocked by pretreatment with a 5-HT 1A antagonist NAD-299 and enhanced by a 5-HT 1A agonist 8-OH-DPAT. However, 5-HT 1B receptor antagonist NAS-181 did not appreciably alter the effects of J147 on depression-like behaviors. Moreover, pretreatment with NAD-299 blocked J147-induced increases in cAMP, PKA, pCREB, and BDNF expression in the hippocampus, while 8-OH-DPAT enhanced the effects of J147 on these proteins’ expression. Conclusion The results suggest that J147 induces rapid antidepressant-like effects during a 3-day treatment period without inducing drug tolerance. These effects might be mediated by 5-HT 1A -dependent cAMP/PKA/pCREB/BDNF signaling.

show abstract

“…In a study carried out on the neurons of db/db mice, it was observed that the pain caused in this condition involves AMP‐activated protein kinase enzyme which upon high glucose increases the expression of transient receptor potential ankyrin 1 (TRPA1), which ultimately mediates pain transduction in diabetic neuropathy (Wang, Wang, Zhou, Qin, & Chen, ). To develop therapeutics, compounds like rutin, curcumin derivative J147, berberine, deguelin, and secretoneurin have been recently tested in animals in which they showed amelioration of diabetic neuropathy (Chen et al, ; Lv, Cao, Zhang, Bai, & Wei, ; Theurl et al, ; Tian et al, ; Zan, Kuai, Qiu, & Huang, ).…”

Section: Introductionmentioning

confidence: 99%

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

View full text Add to dashboard Cite

Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same.

show abstract

A curcumin derivative J147 ameliorates diabetic peripheral neuropathy in streptozotocin (STZ)-induced DPN rat models through negative regulation AMPK on TRPA1

Cited by 18 publications

References 27 publications

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

Sub-Acute Treatment of Curcumin Derivative J147 Ameliorates Depression-Like Behavior Through 5-HT1A-Mediated cAMP Signaling

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Contact Info

Product

Resources

About