SNEDDS curcumin formulation leads to enhanced protection from pain and functional deficits associated with diabetic neuropathy: An insight into its mechanism for neuroprotection

Joshi, Rayanta P.; Negi, Geeta; Kumar, Ashutosh; Pawar, Yogesh B.; Munjal, Bhushan; Bansal, Arvind K.; Sharma, Shyam Sunder

doi:10.1016/j.nano.2013.01.001

Cited by 120 publications

(63 citation statements)

References 35 publications

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“…Similarly, utilizing R98C MPZ mutant mice, it was reported that curcumin mitigates peripheral neuropathy through alleviating ER stress (Patzko et al, 2012). In independent studies, curcumin relieved neuropathic pain induced by toxins or diabetes (Al Moundhri et al, 2013; Babu et al, 2015; Joshi et al, 2013; Zhao et al, 2014). While these positive reports in rodents are encouraging, various studies indicate that curcumin has a poor bioavailability, which limits its use in controlled clinical trials.…”

Section: Small Molecule Therapiesmentioning

confidence: 99%

Promoting peripheral myelin repair

Zhou

Notterpek

2016

Experimental Neurology

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Compared to the central nervous system (CNS), peripheral nerves have a remarkable ability to regenerate and remyelinate. This regenerative capacity to a large extent is dependent on and supported by Schwann cells, the myelin-forming glial cells of the peripheral nervous system (PNS). In a variety of paradigms, Schwann cells are critical in the removal of the degenerated tissue, which is followed by remyelination of newly-regenerated axons. This unique plasticity of Schwann cells has been the target of myelin repair strategies in acute injuries and chronic diseases, such as hereditary demyelinating neuropathies. In one approach, the endogenous regenerative capacity of Schwann cells is enhanced through interventions such as exercise, electrical stimulation or pharmacological means. Alternatively, Schwann cells derived from healthy nerves, or engineered from different tissue sources have been transplanted into the PNS to support remyelination. These transplant approaches can then be further enhanced by exercise and/or electrical stimulation, as well as by the inclusion of biomaterial engineered to support glial cell viability and neurite extension. Advances in our basic understanding of peripheral nerve biology, as well as biomaterial engineering, will further improve the functional repair of myelinated peripheral nerves.

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Section: Small Molecule Therapiesmentioning

confidence: 99%

Promoting peripheral myelin repair

Zhou

Notterpek

2016

Experimental Neurology

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“…Curcumin has anti-inflammatory, anti-oxidant, and neuroprotective properties, which are all potential contributors to the pathogenesis of diabetic neuropathy (Calcutt et al, 2009). Previous studies have shown that curcumin is effective in treating hyperalgesia, large fiber conduction slowing and central nervous system dysfunction in rodent models of diabetes (Ho et al, 2016; Joshi et al, 2013; Peeyush Kumar et al, 2011; Sharma et al, 2007), making curcumin a plausible therapeutic candidate for diabetic neuropathy. Unfortunately, curcumin demonstrates poor bioavailability and blood brain barrier permeability.…”

Section: Introductionmentioning

confidence: 99%

A novel curcumin derivative for the treatment of diabetic neuropathy

et al. 2018

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Neuropathy is a common complication of long-term diabetes. Proposed mechanisms of neuronal damage caused by diabetes that are downstream of hyperglycemia and/or loss of insulin signaling include ischemic hypoxia, inflammation and loss of neurotrophic support. The curcumin derivative J147 is a potent neurogenic and neuroprotective drug candidate initially developed for the treatment of neurodegenerative conditions associated with aging that impacts many pathways implicated in the pathogenesis of diabetic neuropathy. Here, we demonstrate efficacy of J147 in ameliorating multiple indices of neuropathy in the streptozotocin-induced mouse model of type 1 diabetes. Diabetes was determined by blood glucose, HbA1c, and insulin levels and efficacy of J147 by behavioral, physiologic, biochemical, proteomic, and transcriptomic assays. Biological efficacy of systemic J147 treatment was confirmed by its capacity to decrease TNFα pathway activation and several other markers of neuroinflammation in the CNS. Chronic oral treatment with J147 protected the sciatic nerve from progressive diabetes-induced slowing of large myelinated fiber conduction velocity while single doses of J147 rapidly and transiently reversed established touch-evoked allodynia. Conduction slowing and allodynia are clinically relevant markers of early diabetic neuropathy and neuropathic pain, respectively. RNA expression profiling suggests that one of the pathways by which J147 imparts its protection against diabetic induced neuropathy may be through activation of the AMP kinase pathway. The diverse biological and therapeutic effects of J147 suggest it as an alternative to the polypharmaceutical approaches required to treat the multiple pathogenic mechanisms that contribute to diabetic neuropathy.

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“…Scientific literature also shows that curcumin possesses anti-diabetic effects and mitigates diabetes complications owing to its potent ability to suppress oxidative stress and inflammation13. However, a major limitation with curcumin use is its low bioavailability14. Curcumin has also been proven effective for ophthalmic use in various ocular pathologies.…”

mentioning

confidence: 99%

Intranasal delivery of nanomicelle curcumin promotes corneal epithelial wound healing in streptozotocin-induced diabetic mice

Guo

et al. 2016

Sci Rep

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Corneal nerves are mainly derived from the ophthalmic branch of the trigeminal ganglion (TG). Corneal neuropathy contributes to epithelial degenerative changes in diabetic keratopathy. Efficient drug delivery to TG may be beneficial for the treatment of diabetic keratopathy. This article described intranasal delivery of nanomicelle curcumin to correct pathophysiological conditions in TG to promote corneal epithelial/nerve wound healing in streptozotocin-induced diabetic mice. A diabetic mice model with corneal epithelium abrasion was established. Ocular topical and/or intranasal nanomicelle curcumin treatments were performed, and treatment efficacy and mechanisms of action were explored. Results showed that intranasal nanomicelle curcumin treatment promoted corneal epithelial wound healing and recovery of corneal sensation. Enhanced accumulation of reactive oxygen species, reduced free radical scavengers, increased mRNA expressions of inflammatory cytokines, and decreased mRNA expressions of neurotrophic factors in the cornea and TG neuron were observed in diabetic mice with corneal epithelium abrasions. Intranasal nanomicelle curcumin treatment effectively recovered these pathophysiological conditions, especially that of the TG neuron, and a strengthened recovery was observed with ocular topical combined with intranasal treatment. These findings indicated that intranasal curcumin treatment effectively helped promote diabetic corneal epithelial/nerve wound healing. This novel treatment might be a promising strengthened therapy for diabetic keratopathy.

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SNEDDS curcumin formulation leads to enhanced protection from pain and functional deficits associated with diabetic neuropathy: An insight into its mechanism for neuroprotection

Cited by 120 publications

References 35 publications

Promoting peripheral myelin repair

Promoting peripheral myelin repair

A novel curcumin derivative for the treatment of diabetic neuropathy

Intranasal delivery of nanomicelle curcumin promotes corneal epithelial wound healing in streptozotocin-induced diabetic mice

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