Antidiabetic effects of Cuscuta reflexa Roxb. in streptozotocin induced diabetic rats

Rath, Diptirani; Kar, Dattatreya; Panigrahi, Sandeep Kumar; Maharana, Laxmidhar

doi:10.1016/j.jep.2016.09.026

Cited by 23 publications

(12 citation statements)

References 13 publications

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“…3 E), metformin also attenuated body weight loss significantly ( Fig. 3 F), which agrees with data reported in the literature (for example, references [57] , [58] , [59] ). These results further demonstrate that complex I's aberrant hyperactivity was induced by persistent high blood glucose.…”

Section: Resultssupporting

confidence: 90%

Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes

Luo

Thangthaeng

et al. 2017

Biochemistry and Biophysics Reports

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It is well established that NADH/NAD+ redox balance is heavily perturbed in diabetes, and the NADH/NAD+ redox imbalance is a major source of oxidative stress in diabetic tissues. In mitochondria, complex I is the only site for NADH oxidation and NAD+ regeneration and is also a major site for production of mitochondrial reactive oxygen species (ROS). Yet how complex I responds to the NADH/NAD+ redox imbalance and any potential consequences of such response in diabetic pancreas have not been investigated. We report here that pancreatic mitochondrial complex I showed aberrant hyperactivity in either type 1 or type 2 diabetes. Further studies focusing on streptozotocin (STZ)-induced diabetes indicate that complex I hyperactivity could be attenuated by metformin. Moreover, complex I hyperactivity was accompanied by increased activities of complexes II to IV, but not complex V, suggesting that overflow of NADH via complex I in diabetes could be diverted to ROS production. Indeed in diabetic pancreas, ROS production and oxidative stress increased and mitochondrial ATP production decreased, which can be attributed to impaired pancreatic mitochondrial membrane potential that is responsible for increased cell death. Additionally, cellular defense systems such as glucose 6-phosphate dehydrogenase, sirtuin 3, and NQO1 were found to be compromised in diabetic pancreas. Our findings point to the direction that complex I aberrant hyperactivity in pancreas could be a major source of oxidative stress and β cell failure in diabetes. Therefore, inhibiting pancreatic complex I hyperactivity and attenuating its ROS production by various means in diabetes might serve as a promising approach for anti-diabetic therapies.

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Section: Resultssupporting

confidence: 90%

Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes

Luo

Thangthaeng

et al. 2017

Biochemistry and Biophysics Reports

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“…STZ is a cytotoxic agent that leads to degeneration of pancreatic beta cells and therefore induces symptoms of type-1 diabetes, i.e., hypoinsulinemia, hyperglycemia, polydipsia, polyuria, and weight loss (2324). In the present study, as expected, insulin could inhibit weight loss and reduced water intake in diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of ethanolic extract of Ferula gummosa oleo-resin in a rat model of streptozotocin-induced diabetes

et al. 2019

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Previous studies have shown that some plants in the genus of Ferula (Apiaceae) have antidiabetic effects. The present work was aimed to evaluate effects of Ferula gummosa oleo-resin in a rat model of streptozotocin-induced diabetes. Male Wistar rats were randomized into five groups (n = 6): normal control, diabetic control, diabetic rats treated with insulin (3 IU/day), and diabetic rats treated with 100 or 400 mg/kg/day of an ethanolic extract of the oleo-resin. After 4 weeks, blood samples were collected for measuring fasting blood glucose (FBG), lipid profile, aspartate aminotransferase, alanine aminotransferase (ALT), alkaline phosphatase, blood urea nitrogen, and creatinine. In addition, levels of lipid peroxidation, thiol groups, and superoxide dismutase (SOD) activity were evaluated in the liver and kidney. At the end of the fourth week, the level of FBG in rats treated with 100 mg/kg of the extract was lower than that in diabetic control rats (273 ± 39 mg/dL vs 471 ± 32 mg/dL). Administration of insulin and the extract had no significant effects on the serum lipids. Insulin and both doses of the extract significantly reduced the activity of ALT. In addition, the extract inhibited lipid peroxidation in the kidney and restored the elevated level of SOD in the liver and kidneys. Ferula gummosa oleo-resin has the potential to prevent or delay the complications of diabetes by inhibiting the progression of hyperglycemia and attenuating oxidative stress-induced damage in the liver and kidneys.

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“…The multiple targeting potential of BSHX in fighting against T2DM -related cognition dysfunction is predictable if consider the data so far available found for the role of the components contained in this preparation. Of them, Cuscuta chinensis Lam has been demonstrated to reduce blood glucose in streptozotocin (STZ) induced diabetic rats (Dao-Zhong et al, 2008 ; Rath et al, 2016 ). The anti-hyperglycemia potential was also reported for Schisandra chinensis (Turcz.)…”

Section: Discussionmentioning

confidence: 99%

Bushen Huoxue Attenuates Diabetes-Induced Cognitive Impairment by Improvement of Cerebral Microcirculation: Involvement of RhoA/ROCK/moesin and Src Signaling Pathways

Pan

et al. 2018

Front. Physiol.

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Type 2 Diabetes mellitus (T2DM) is closely correlated with cognitive impairment and neurodegenerative disease. Bushen Huoxue (BSHX) is a compound Chinese medicine used clinically to treat diabetes-induced cognitive impairment. However, its underlying mechanisms remain unclear. In the present study, KKAy mice, a genetic model of type 2 diabetes with obesity and insulin resistant hyperglycemia, received a daily administration of BSHX for 12 weeks. Blood glucose was measured every 4 weeks. After 12 weeks, BSHX treatment significantly ameliorated the T2DM related insults, including the increased blood glucose, the impaired spatial memory, decreased cerebral blood flow (CBF), occurrence of albumin leakage, leukocyte adhesion and opening capillary rarefaction. Meanwhile, the downregulation of the tight junction proteins (TJ) claudin-5, occludin, zonula occluden-1 (ZO-1) and JAM-1 between endothelial cells, amyloid-β (Aβ) accumulation in hippocampus, increased AGEs and RAGE, and expression of RhoA/ROCK/moesin signaling pathway and phosphorylation of Src kinase in KKAy mice were significantly protected by BSHX treatment. These results indicate that the protective effect of BSHX on T2DM-induced cognitive impairment involves regulation of RhoA/ROCK1/moesin signaling pathway and phosphorylation of Src kinase.

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Antidiabetic effects of Cuscuta reflexa Roxb. in streptozotocin induced diabetic rats

Cited by 23 publications

References 13 publications

Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes

Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes

Effects of ethanolic extract of Ferula gummosa oleo-resin in a rat model of streptozotocin-induced diabetes

Bushen Huoxue Attenuates Diabetes-Induced Cognitive Impairment by Improvement of Cerebral Microcirculation: Involvement of RhoA/ROCK/moesin and Src Signaling Pathways

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