Diabetic Peripheral Neuropathy: Role of Reactive Oxygen and Nitrogen Species

Premkumar, Louis S.; Pabbidi, Reddy M.

doi:10.1007/s12013-013-9609-5

Cited by 38 publications

(32 citation statements)

References 123 publications

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“…Next, we investigated on the mechanism of cell death. From the earlier studies and in a condition like hyperglycemia, it is well known that excessive influx of glucose can lead to over loading of the mitochondrial electron transport chain (ETC) resulting in the excessive ROS (Fernyhough & Calcutt, 2010;Fernyhough, Roy Chowdhury, & Schmidt, 2010;Gonzalez et al, 2016;Naziroglu, Dikici, & Dursun 2012;Premkumar & Pabbidi, 2013). However it has be noted that excessive inflammation which is also observed in prolonged hyperglycemia results in oxidative stress (Haidara, Yassin, Rateb, Ammar, & Zorkani, 2006).…”

Section: Increase In Basal [Ca 2+ ] I Mediated Ros Is Key Determinamentioning

confidence: 99%

MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines

Chandramoorthy

Bin-Jaliah

Karari

et al. 2017

Journal Cellular Physiology

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The MSCs of various origins are known to ameliorate or modulate cell survival strategies. We investigated, whether UCB MSCs could improve the survival of the human neuronal cells and/or fibroblast assaulted with DPN sera. The results showed, the co-culture of UCB MSCs with human neuronal cells and/or fibroblasts could effectively scavenge the pro-inflammatory cytokines TNF-α, IL-1β, IFN-ɤ and IL - 12 and control the pro-apoptotic expression of p53/Bax. Further co-culture of UCB MSCs have shown to induce anti-inflammatory cytokines like IL-4, IL-10 and TGF-β and anti-apoptotic Bclxl/Bcl2 expression in the DPN sera stressed cells. Amelioration of elevated [Ca ] and cROS, the portent behind the NFκB/Caspase-3 mediated inflammation in DPN rescued the cells from apoptosis. The results of systemic administration of BM MSCs improved DPN pathology in rat as extrapolated from human cell model. The BM MSCs ameliorated prolonged distal motor latency (control: 0.70 ± 0.06, DPN: 1.29 ± 0.13 m/s DPN + BM MSCs: 0.89 ± 0.02 m/s, p < 0.05) and lowered high amplitude of compound muscle action potentials (CMAPs) (control: 12.36 ± 0.41, DPN: 7.52 ± 0.61 mV, DPN + MSCs: 8.79 ± 0.53 mV, p < 0.05), while slowly restoring the plasma glucose levels. Together, all these results showed that administration of BM or UCB MSCs improved the DPN via ameliorating pro-inflammatory cytokine signaling and [Ca ] homeostasis.

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Section: Increase In Basal [Ca 2+ ] I Mediated Ros Is Key Determinamentioning

confidence: 99%

MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines

Chandramoorthy

Bin-Jaliah

Karari

et al. 2017

Journal Cellular Physiology

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“…Insulin is the primary stabilizer of the carbohydrate metabolism and has significant effects on and associations with other metabolic activities. Hyperglycaemia can cause cellular damage that creates losses in the structure and function of systems, organs, and tissues, such as the nervous system, kidney, and salivary glands [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Effects of Diabetes on Post-Menopausal Rat Submandibular Glands: A Histopathological and Stereological Examination

et al. 2015

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Objective: The menopause in elderly women is a physiological process where ovarian and uterine cycles end. Diabetes means higher blood glucose level that is a metabolic disease and has an increased incidence. The aim of the study was to examine the single or combined effects of menopause and diabetes that causes pathophysiological processes on submandibular gland on ovariectomy and diabetes induced rat models. Materials and Methods:Sprague Dawley twelve weeks old female (n=24) rats were divided randomly into four groups; Healthy control group (n=6), diabetic group (DM, n=6), ovariectomized group (OVX, n=6), post ovariectomy diabetes induced group (DM+OVX, n=6) individually. Histopathological, histochemical and stereological analyses were done in these groups.Results: Significant neutrophil cell infiltrations and myoepithelial cell proliferations, granular duct and seromucous acini damages and changes in the content of especially seromucous acini secretion in DM and/or OVX groups and distinctive interstitial and striated duct damages in post ovariectomy diabetes induced group were detected. Alterations ingranular ducts hypertrophic and in seromucous acini atrophic were determined in DM and/or OVX groups. Conclusion:The results revealed the pathophysiological processes that lead to morphological and functional alterations on the cellular level in submandibular glands. The molecular mechanisms related with pathogenesis of diabetes and menopause need further investigation.Keywords: Diabetes, gland, menopause, rat, submandibular ÖzetAmaç: İlerleyen yaş ile birlikte, menopoz, kadınlarda gözlenen overial ve menstrual sikluslarda azalma veya bitiş ile karakterize fizyolojik bir süreç ve diyabet ise insidansı artan yüksek kan şekeri seviyesi ile karakterize metabolik hastalıktır. Overektomi ve diyabet indüklenen sıçan modelleri submandibular bezi üzerinde menopozun ve diyabetin tek veya kombine etkilerinin neden olduğu patofizyolojik süreçle-ri incelemek amacı ile çalışma tasarlandı. Gereç ve Yöntem:Sprague Dawley on iki haftalık dişi (n=24) sıçanlar dört gruba randomize bir şekilde rastgele ayrıldı; Sağlıklı Kontrol Grubu (n=6), Diyabetik grup (n=6), Overektomize grup (n=6), Post Overektomize Diyabet İndüklenen Grup (n=6). Sonuçlar histopatolojik, histokimyasal ve stereolojik analizler ile değerlendirildi. Bulgular:Anlamlı nötrofil infiltrasyonları ve myoepitel hücre proliferasyonları, granüler kanal ve seromuköz hücre dejenerasyonları ve özellikle seromuköz asinusların salgısı içeriğindeki değişimler DM ve/veya OVX gruplarında, belirgin intersistiyel ödem ve çizgili kanal dejenerasyonları diyabet indüklenen post overektomize grup submandibular dokularında izlendi. Granular kanallarda hipertrofik değişiklikler, seromuköz asinuslarda atrofik değişiklikler DM ve/veya OVX gruplarında tespit edildi.Sonuç: Diyabet ve overektominin submandibular bezlerinde yol açtığı patofizyolojik süreçlere bağlı hücresel düzeyde morfolojik ve fonksiyonel değişiklikler gösterildi. Diyabet ve menopozun patogenezi ile ilişkili moleküle...

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“…Oxidative stress is considered to be an imbalance between the production of ROS and activated anti-oxidative mechanisms in cells (28). Hyperglycemia-induced overproduction of free radicals is considered to be the source of DPN complication through increased glycolysis (29).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of hydrogen-rich medium against high glucose-induced apoptosis of Schwann cells in vitro

Yang

et al. 2015

Molecular Medicine Reports

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Diabetic peripheral neuropathy (DPN) is considered to be one of the most prevalent and life threatening microvascular diabetic complications. DPN affects up to 50% of patients with diabetes mellitus and there are currently no efficacious therapeutic strategies available for its treatment. Previous studies have reported that oxidative stress and poly(ADP‑ribose) polymerase‑1 (PARP‑1) may be unifying factors for hyperglycemic injury. The aim of the present study was to investigate the protective effects of hydrogen‑rich medium (HM) on high glucose (HG)‑mediated oxidative stress, PARP‑1 activation and the apoptosis of Schwann cells (SCs) in vitro. The cells were divided into different groups, and were treated for 48 h. Cell viability and apoptosis were evaluated using Cell Counting kit‑8 and annexin V/propidium iodide assays, respectively. The concentrations of 8‑hydroxy‑2‑deoxyguanosine (8‑OHdG) and peroxynitrite (ONOO‑) were detected using an enzyme‑linked immunosorbent assay. The presence of intracellular oxygen free radicals was confirmed using flow cytometric analysis. Colorimetric assays were performed to determine the activity of caspase‑3, and western blotting was performed to detect the protein expression levels of PARP‑1, cleaved PARP‑1, PAR, apoptosis‑inducing factor (AIF), B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein. HG was found to induce severe oxidative stress and promote the caspase‑dependent and caspase‑independent apoptosis of SCs. Treatment with HM inhibited HG‑induced oxidative stress by suppressing hydroxyl and ONOO‑ production, levels of 8‑OHdG, caspase‑3 activity and apoptosis in the SCs. Furthermore, treatment with HM downregulated the HG‑induced release of PAR, the activation of PARP‑1 and nuclear translocation of AIF, and upregulated the expression of Bcl‑2 in the SCs. These results indicated that HM inhibited the HG‑induced‑oxidative stress‑associated caspase‑dependent and caspase‑independent apoptotic pathways in SCs. Therefore, HM may have potential as a treatment for DPN.

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Diabetic Peripheral Neuropathy: Role of Reactive Oxygen and Nitrogen Species

Cited by 38 publications

References 123 publications

MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines

MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines

Effects of Diabetes on Post-Menopausal Rat Submandibular Glands: A Histopathological and Stereological Examination

Protective effect of hydrogen-rich medium against high glucose-induced apoptosis of Schwann cells in vitro

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Diabetic Peripheral Neuropathy: Role of Reactive Oxygen and Nitrogen Species

Cited by 38 publications

References 123 publications

MSCs ameliorates DPN induced cellular pathology via [Ca2+]i homeostasis and scavenging the pro‐inflammatory cytokines

MSCs ameliorates DPN induced cellular pathology via [Ca2+]i homeostasis and scavenging the pro‐inflammatory cytokines

Effects of Diabetes on Post-Menopausal Rat Submandibular Glands: A Histopathological and Stereological Examination

Protective effect of hydrogen-rich medium against high glucose-induced apoptosis of Schwann cells in vitro

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MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines

MSCs ameliorates DPN induced cellular pathology via [Ca²⁺]_i homeostasis and scavenging the pro‐inflammatory cytokines