Taurine protects against myelin damage of sciatic nerve in diabetic peripheral neuropathy rats by controlling apoptosis of schwann cells via NGF/Akt/GSK3β pathway

Li, Kaixin; Shi, Xiaoxia; Luo, Ming; Inamullah, .; Wu, Pingan; Zhang, Mengren; Zhang, Cong; Li, Qiujuan; Wang, Yachen; Piao, Fengyuan

doi:10.1016/j.yexcr.2019.111557

Cited by 29 publications

(23 citation statements)

References 41 publications

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“…The mice were fed standard rodent chow (NMF; Oriental Yeast Co. Ltd., Tokyo, Japan). Several studies were performed with 1% (w/v) taurine containing water (Kim et al, 2017;Li et al, 2019;Park et al, 2017). In the present study, mice were given 0.5% (w/v) or 2% (w/v) taurine in their drinking water for four weeks.…”

Section: Animal Treatment Sample Collection and Histological Analysismentioning

confidence: 98%

Taurine attenuates hepatic steatosis in a genetic model of fatty liver disease

et al. 2020

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Mice lacking the farnesoid X receptor (FXR) are used as a genetic model for nonalcoholic fatty liver disease because their livers exhibit hepatic steatosis and inflammation. The influence of taurine drinking on disrupted hepatic function was investigated using female Fxr-null mice. Significant decreases in the levels of hepatic damage-associated diagnostic markers, hepatic triglycerides, non-esterified fatty acids, and total bile acids were found in Fxr-null mice that had drunk water containing 0.5% taurine for four weeks. Hepatic but not serum taurine concentrations were significantly increased in these mice. The expression levels of oxidative stress-related genes (Hmox1 and Gsta1) and fatty acid synthetic genes (Acc1 and Scd1) were significantly decreased in these mice. These results suggest that drinking taurine improves hepatic steatosis and dysfunction caused by a lack of FXR.

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Section: Animal Treatment Sample Collection and Histological Analysismentioning

confidence: 98%

Taurine attenuates hepatic steatosis in a genetic model of fatty liver disease

et al. 2020

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“…Schwann cells are very sensitive to glucose and insulin levels and closely involved in DPN pathogenesis. Numerous reports have demonstrated that hyperglycemia causes Schwann cell apoptosis during the development of DPN [ 10 , 11 , 12 , 13 ]. Schwann cells play a crucial role in DPN pathogenic mechanisms and are thus an important therapeutic target for diabetic neuropathy [ 7 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Cheng

Chu²,

Chen

et al. 2020

Cells

109

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Diabetic peripheral neuropathy (DPN) is caused by hyperglycemia, which induces oxidative stress and inflammatory responses that damage nerve tissue. Excessive generation of reactive oxygen species (ROS) and NOD-like receptor protein 3 (NLRP3) inflammasome activation trigger the inflammation and pyroptosis in diabetes. Schwann cell dysfunction further promotes DPN progression. Loganin has been shown to have antioxidant and anti-inflammatory neuroprotective activities. This study evaluated the neuroprotective effect of loganin on high-glucose (25 mM)-induced rat Schwann cell line RSC96 injury, a recognized in vitro cell model of DPN. RSC96 cells were pretreated with loganin (0.1, 1, 10, 25, 50 μM) before exposure to high glucose. Loganin’s effects were examined by CCK-8 assay, ROS assay, cell death assay, immunofluorescence staining, quantitative RT–PCR and western blot. High-glucose-treated RSC96 cells sustained cell viability loss, ROS generation, NF-κB nuclear translocation, P2 × 7 purinergic receptor and TXNIP (thioredoxin-interacting protein) expression, NLRP3 inflammasome (NLRP3, ASC, caspase-1) activation, IL-1β and IL-18 maturation and gasdermin D cleavage. Those effects were reduced by loganin pretreatment. In conclusion, we found that loganin’s antioxidant effects prevent RSC96 Schwann cell pyroptosis by inhibiting ROS generation and suppressing NLRP3 inflammasome activation.

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“…Previous studies have demonstrated that apoptosis of SCs induced by high glucose contributes to the development of DPN [12][13][14][15]. Effective drugs to prevent apoptosis of SCs are important for relieving and reversing peripheral nerve injury caused by DM.…”

Section: Discussionmentioning

confidence: 99%

“…For the control conditions, 45 μ M mannitol was used to match the hyperosmolality of the cells cultured in the hyperglycemic conditions. The glucose concentrations and oltipraz concentrations used in the present study were based on previous studies [ 15 , 31 ].…”

Section: Methodsmentioning

confidence: 99%

“…SC apoptosis induced by a high glucose environment is thought to be one of the primary causes of DPN. Increased SC apoptosis was observed in diabetic (db/db) mice and diabetic rats treated with streptozotocin [ 12 – 15 ]. A previous study showed that inhibiting SC apoptosis could alleviate myelin sheath injury and delay peripheral nerve degeneration in DPN [ 15 – 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

Jiang

Bian

et al. 2020

BioMed Research International

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Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). Schwann cell (SC) apoptosis contributes to the occurrence and development of DPN. Effective drugs to prevent SC apoptosis are required to relieve and reverse peripheral nerve injury caused by DM. Oltipraz [4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione], an agonist of nuclear factor erythroid derived-2-related factor 2 (Nrf2), exerts strong effect against oxidative stress in animal models or clinical patients in certain diseases, including heart failure, acute kidney injury, and liver injury. The aim of the present study was to determine the effectiveness of oltipraz in preventing SC apoptosis induced by high glucose levels. RSC96 cells pretreated with oltipraz were cultured in high-glucose medium (50 mM glucose) for 24 h, and cells cultured in medium containing 5 mM glucose were used as the control. Flow cytometry was used to evaluate the degree of apoptosis. A Cell Counting Kit-8 assay was used to assess cell viability. The mitochondrial membrane potential was assessed using JC-1 staining, and reactive oxygen species (ROS) generation was measured using 20,70-dichlorodihydrofluorescein diacetate staining. In addition, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) levels were also evaluated using the corresponding kits. Flow cytometry was subsequently used to detect apoptosis, and western blotting was used to measure the expression levels of nuclear factor erythroid derived-2-related factor 2 and NADPH quinone oxidoreductase 1. The results showed that high glucose concentration increased oxidative stress and apoptosis in RSC96 cells. Oltipraz improved cell viability and reduced apoptosis of RSC96 cells in the high glucose environment. Additionally, oltipraz exhibited a significant antioxidative effect, as shown by the decrease in MDA levels, increased SOD levels, and reduced ROS generation in RSC96 cells. The results of the present study suggest that oltipraz exhibits potential as an effective drug for treatment with DPN.

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Taurine protects against myelin damage of sciatic nerve in diabetic peripheral neuropathy rats by controlling apoptosis of schwann cells via NGF/Akt/GSK3β pathway

Cited by 29 publications

References 41 publications

Taurine attenuates hepatic steatosis in a genetic model of fatty liver disease

Taurine attenuates hepatic steatosis in a genetic model of fatty liver disease

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

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