Neuroactive steroids and diabetic complications in the nervous system

Giatti, Silvia; Mastrangelo, R; D’Antonio, Maurizio; Pesaresi, Marzia; Romano, Simone; Diviccaro, Silvia; Caruso, Donatella; Mitro, Nico; Melcangi, Roberto Cosimo

doi:10.1016/j.yfrne.2017.07.006

Cited by 30 publications

(21 citation statements)

References 184 publications

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“…Diabetes is a key cause of cardiovascular disease, retinal disease, and the development and progression of neurological diseases. 44 DE is a series of behavioural and pathological changes caused by constitutive hyperglycaemia, including cognitive decline, neuronal loss and disorders of glycolipid metabolism. [45][46][47] DE decreased the patient's ability of the learning and memory.…”

Section: Discussionmentioning

confidence: 99%

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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Epidemiological studies have found that diabetes and cognitive dysfunction are closely related. Quercetin has been certified with the effect on improving diabetes mellitus (DM) and cognitive impairment. However, the effect and related mechanism of quercetin on diabetic encephalopathy (DE) are still ambiguous. In this study, we used the db/db mice (diabetic model) to discover whether quercetin could improve DE through the Sirtuin1/NLRP3 (NOD‐, LRR‐ and pyrin domain‐containing 3) pathway. Behavioural results (Morris water maze and new object recognition tests) showed that quercetin (70 mg/kg) improved the learning and memory. Furthermore, quercetin alleviated insulin resistance and the level of fasting blood glucose. Besides, Western blot analysis also showed that quercetin increased the protein expressions of nerve‐ and synapse‐related protein, including postsynapticdensity 93 (PSD93), postsynapticdensity 95 (PSD95), brain‐derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brain of db/db mice. Quercetin also increased the protein expression of SIRT1 and decreased the expression of NLRP3 inflammation‐related proteins, including NLRP3, the adaptor protein ASC and cleaved Caspase‐1, the pro‐inflammatory cytokines IL‐1β and IL‐18. In conclusion, the present results indicate that the SIRT1/NLRP3 pathway may be a crucial mechanism for the neuroprotective effect of quercetin against DE.

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Section: Discussionmentioning

confidence: 99%

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Diabetes can cause many organic complications as a result of neuropathies and angiopathies [ 1 – 3 , 12 ]. The association between hearing loss and diabetes is not well known; however, several reports have shown that diabetes is associated with, and a potential risk factor for, hearing loss.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Diabetes is a representative metabolic disease that results in many complications [ 1 – 3 ]. In general, patients with diabetes are prone to inflammatory diseases and increased inflammatory responses in many organs [ 4 – 11 ] and are more vulnerable to trauma and tissue injuries in end organs [ 1 , 3 , 12 – 14 ]. Diabetes per se is regarded as a risk factor of many inflammatory diseases and trauma due to disrupted homeostasis and immune responses [ 4 – 6 , 9 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Susceptibility of Diabetic Mice to Noise Trauma

Han

Kim

Shin

et al. 2018

BioMed Research International

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Diabetes can lead to many end-organ complications. However, the association between diabetes and hearing loss is not well understood. Here, we investigated the effect of noise exposure on diabetic mice compared with wild-type mice. Hearing threshold shifts, histopathologic changes in the cochlea, and inflammatory responses were evaluated over time. After noise exposure, more severe hearing threshold shifts, auditory hair cell loss, and synaptopathies were notable in diabetic mice compared with wild-type mice. Moreover, increased inflammatory responses and reactive oxygen species production were observed in the ears of diabetic mice. The results demonstrated that diabetic mice are more susceptible to noise trauma.

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“…Aging 36 is the result of biological events that progressively and irreversibly compromise the function of vital organs. The related pathophysiological changes include cancer, [37][38][39] cardiovascular diseases, [40][41][42] neurological diseases, [43][44][45] metabolic syndrome, [46][47][48] and motor system diseases. 20 Osteoporosis is a debilitating chronic bone disease accompanied by increased bone loss and a high risk of fracture and is F I G U R E 1 Signaling network of osteogenesis and osteolysis.…”

Section: Melatonin Maintains Metabolic Homeostasis In Bonementioning

confidence: 99%

Melatonin: Another avenue for treating osteoporosis?

Tian

Jiang

et al. 2019

Journal of Pineal Research

109

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Melatonin is a signal molecule that modulates the biological circadian rhythms of vertebrates. Melatonin deficiency is thought to be associated with several disorders, including insomnia, cancer, and cardiovascular and neurodegenerative diseases. Accumulating evidence has also indicated that melatonin may be involved in the homeostasis of bone metabolism. Age‐related reductions in melatonin are considered to be critical factors in bone loss and osteoporosis with aging. Thus, serum melatonin levels might serve as a biomarker for the early detection and prevention of osteoporosis. Compared to conventional antiosteoporosis medicines, which primarily inhibit bone loss, melatonin both suppresses bone loss and promotes new bone formation. Mechanistically, by activating melatonin receptor 2 (MT2), melatonin upregulates the gene expression of alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP2), BMP6, osteocalcin, and osteoprotegerin to promote osteogenesis while inhibiting the receptor activator of NF‐kB ligand (RANKL) pathway to suppress osteolysis. In view of the distinct actions of melatonin on bone metabolism, we hypothesize that melatonin may be a novel remedy for the prevention and clinical treatment of osteoporosis.

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Neuroactive steroids and diabetic complications in the nervous system

Cited by 30 publications

References 184 publications

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Susceptibility of Diabetic Mice to Noise Trauma

Melatonin: Another avenue for treating osteoporosis?

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