scholarly journals Chondroitin Sulfate Alleviates Diabetic Osteoporosis and Repairs Bone Microstructure via Anti-Oxidation, Anti-Inflammation, and Regulating Bone Metabolism

2021 ◽  
Vol 12 ◽  
Author(s):  
Shan Shan Qi ◽  
Meng Li Shao ◽  
Ze Sun ◽  
Si Min Chen ◽  
Ying Jun Hu ◽  
...  
Keyword(s):  
Chondroitin Sulfate ◽  
Bone Metabolism ◽  
Bone Microstructure ◽  
Diabetic Rats ◽  
Activity Level ◽  
Diabetic Rat ◽  
High Morbidity ◽  
Mineral Density ◽  
Sod Activity ◽  
Diabetic Osteoporosis

Diabetic osteoporosis (DOP) belongs to secondary osteoporosis caused by diabetes; it has the characteristics of high morbidity and high disability. In the present study, we constructed a type 1 diabetic rat model and administered chondroitin sulfate (200 mg/kg) for 10 weeks to observe the preventive effect of chondroitin sulfate on the bone loss of diabetic rats. The results showed that chondroitin sulfate can reduce blood glucose and relieve symptoms of diabetic rats; in addition, it can significantly increase the bone mineral density, improve bone microstructure, and reduce bone marrow adipocyte number in diabetic rats; after 10 weeks of chondroitin sulfate administration, the SOD activity level was upregulated, as well as CAT levels, indicating that chondroitin sulfate can alleviate oxidative stress in diabetic rats. Chondroitin sulfate was also found to reduce the level of serum inflammatory cytokines (TNF-α, IL-1, IL-6, and MCP-1) and alleviate the inflammation in diabetic rats; bone metabolism marker detection results showed that chondroitin sulfate can reduce bone turnover in diabetic rats (decreased RANKL, CTX-1, ALP, and TRACP 5b levels were observed after 10 weeks of chondroitin sulfate administration). At the same time, the bone OPG and RUNX 2 expression levels were higher after chondroitin sulfate treatment, the bone RANKL expression was lowered, and the OPG/RANKL ratio was upregulated. All of the above indicated that chondroitin sulfate could prevent STZ-induced DOP and repair bone microstructure; the main mechanism was through anti-oxidation, anti-inflammatory, and regulating bone metabolism. Chondroitin sulfate could be used to develop anti-DOP functional foods and diet interventions for diabetes.

scholarly journals Chondroitin Sulfate Prevents STZ Induced Diabetic Osteoporosis through Decreasing Blood Glucose, AntiOxidative Stress, Anti-Inflammation and OPG/RANKL Expression Regulation

2020 ◽  
Vol 21 (15) ◽  
pp. 5303 ◽  
Author(s):  
Hong Xing Zheng ◽  
De Jing Chen ◽  
Yue Xin Zu ◽  
En Zhu Wang ◽  
Shan Shan Qi
Keyword(s):  
Blood Glucose ◽  
Chondroitin Sulfate ◽  
Treated Group ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Rankl Expression ◽  
Mineral Density ◽  
Diabetic Osteoporosis ◽  
Antioxidative Stress ◽  
Anti Inflammation

Chondroitin sulfate (CS) has antioxidative, anti-inflammatory, anti-osteoarthritic and hypoglycemic effects. However, whether it has antidiabetic osteoporosis effects has not been reported. Therefore, in this study, we established a STZ-induced diabetic rat model; CS (500 mg kg−1 d−1) was orally administrated for eight weeks to study its preventive effects on diabetic osteoporosis. The results showed that eight weeks of CS treatment improved the symptoms of diabetes; the CS-treated group has increased body weight, decreased water or food intake, decreased blood glucose, increased bone-mineral density, repaired bone morphology and decreased femoral osteoclasts and tibia adipocytes numbers. After CS treatment, bone histomorphometric parameters returned to normal, the levels of serum inflammatory cytokines (IL-1β, IL-6 and TNF-α) decreased significantly, serum SOD, GPX and CAT activities increased and MDA level increased. In the CS-treated group, the levels of serum ALP, CTX-1, TRACP 5b, osteocalcin and RANKL decreased and the serum RUNX 2 and OPG levels increased. Bone immunohistochemistry results showed that CS can effectively increase the expression of OPG and RUNX2 and reduce the expression of RANKL in diabetic rats. All of these indicate that CS could prevent STZ induced diabetic osteoporosis—mainly through decreasing blood glucose, antioxidative stress, anti-inflammation and regulation of OPG/RANKL expression. CS can therefore effectively prevent bone loss caused by diabetes.

scholarly journals Mechanism bySambucus nigraExtract Improves Bone Mineral Density in Experimental Diabetes

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Laurentiu Badescu ◽  
Oana Badulescu ◽  
Magda Badescu ◽  
Manuela Ciocoiu
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
Mineral Content ◽  
Diabetic Rats ◽  
Mineral Density ◽  
Sambucus Nigra ◽  
Polyphenolic Extract ◽  
Before And After ◽  
Total Antioxidant ◽  
Diabetic Osteoporosis

The effects of polyphenols extracted fromSambucus nigrafruit were studied in streptozotocin- (STZ-) induced hyperglycemic rats to evaluate its possible antioxidant, anti-inflammatory, antiglycosylation activity, and antiosteoporosis effects in diabetes. DEXA bone mineral density tests were performed in order to determine bone mineral density (BMD), bone mineral content (BMC), and fat (%Fat) in control and diabetic animals, before and after polyphenol delivery. As compared to the normoglycemic group, the rats treated with STZ (60 mg/kg body weight) revealed a significant malondialdehyde (MDA) increase, as an index of the lipid peroxidation level, by 69%, while the total antioxidant activity (TAS) dropped by 36%, with a consistently significant decrease () in the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPX). Also, the treatment of rats with STZ revealed a significant increase of IL-6, glycosylated haemoglobin (HbA1c), and osteopenia detected by DEXA bone mineral density tests. The recorded results highlight a significant improvement () in the antioxidative capacity of the serum in diabetic rats treated with natural polyphenols, bringing back to normal the concentration of reduced glutathione (GSH), as well as an important decrease in the serum concentration of MDA, with improved osteoporosis status. Knowing the effects of polyphenols could lead to the use of the polyphenolic extract ofSambucus nigraas a dietary supplement in diabetic osteoporosis.

T1081 The Effect of PPI (Proton Pump Inhibitor) on the Bone Mineral Density, Bone Microstructure and Bone Metabolism of Rat

2010 ◽  
Vol 138 (5) ◽  
pp. S-484
Author(s):  
Moon Kyung Joo ◽  
Jong-Jae Park ◽  
Beom Jae Lee ◽  
Jong Yeol Kim ◽  
Jin Ki Hwang ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Proton Pump Inhibitor ◽  
Bone Metabolism ◽  
Bone Mineral ◽  
Proton Pump ◽  
Bone Microstructure ◽  
Mineral Density

scholarly journals Islet Transplantation Attenuating Testicular Injury in Type 1 Diabetic Rats Is Associated with Suppression of Oxidative Stress and Inflammation via Nrf-2/HO-1 and NF-κB Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Xiandong Zhu ◽  
Feixia Guo ◽  
Hengjie Tang ◽  
Chongchu Huang ◽  
Gangyin Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Islet Transplantation ◽  
Group Versus ◽  
Myocardial Damage ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Testicular Damage ◽  
Sod Activity ◽  
Respective Treatment ◽  
Testicular Injury

Testicular structural and functional impairment is a serious complication in male diabetes mellitus (DM) patients that leads to impaired fertility in adulthood. In contrast to other endocrine therapies, islet transplantation (IT) can effectively prevent and even reverse diabetic nephropathy and myocardial damage. However, whether IT can alleviate diabetes-induced testicular injury remains unclear. In this study, we sought to investigate the effect of IT on diabetes-induced testicular damage. A diabetic rat model was established by streptozotocin injection. DM, IT, and insulin treatment (INS) groups were compared after 4 weeks of respective treatment. We confirmed that IT could effectively attenuate diabetes-induced testicular damage and recover sperm counts more extensively compared with INS in diabetic rats. In addition, significantly higher levels of superoxide dismutase (SOD) activity and lower contents of malondialdehyde (MDA) were detected in the testes of the IT group versus diabetic rats. Mechanism studies revealed that IT significantly activates the expression of Nrf-2, HO-1, and NQO-1 and inhibits upregulation of the NF-κB expression in response to DM, while INS only exhibit slight impact on the protein expression. Therefore, we speculate that IT may prevent the progression of testicular damage by downregulating oxidative stress and inhibiting inflammation via Nrf-2/HO-1 and NF-κB pathways.

scholarly journals Anethum graveolens L‎. Alleviates Sperm ‎Damage by Limiting Oxidative Stress ‎and Insulin ‎Resistance ‎in ‎Diabetic Rats ‎

2020 ◽  
Vol 14 (1) ◽  
pp. 35-44
Author(s):  
Ebrahim Abbasi-Oshaghi ◽  
Iraj Khodadadi ◽  
Fatemeh Mirzaei ◽  
Mehrdad Ahmadi ◽  
Heidar Tayebinia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Morphological Changes ◽  
Diabetic Rats ◽  
Male Rats ◽  
Diabetic Rat ◽  
Anethum Graveolens ◽  
Sod Activity ◽  
Histological Changes ◽  
Anti Oxidant

Background: It has been reported that diabetes is associated with sperm ‎damage and infertility. Objective: The purpose of this experiment was to survey the effect of Anethum graveolens L. (Dill) powder on sperm profiles, oxidative stress, insulin resistance, and histological changes in male diabetic rats. Methods: Male rats were randomly divided into 6 groups (n=7); group 1: normal rats, 2: normal rats + 100mg/kg Dill, 3: normal rats + 300mg/kg Dill, 4: diabetic rats, 5: diabetic rats + 100mg/kg Dill, and 6: diabetic rats + 300mg/kg Dill. After 2 months of treatments, the sperm profile, anti-oxidant activity, superoxide dismutase (SOD) activity, and malondialdehyde were measured. The histopathology of testis was evaluated. Hormonal changes and tumor necrosis factor-α (TNF-α) levels were measured by ELISA. Results: Total anti-oxidant and SOD activity in diabetic rats significantly decreased, while MDA concentration was significantly increased in the testis and pancreas of diabetic rats compared with control. However, the use of Dill significantly normalized these profiles. The treatment of diabetic rats with Dill changed the sperm parameters. The levels of testosterone, FSH, and LH in diabetic rats were significantly reduced, but the treatment with Dill did not alter the level of these hormones. Dill also significantly normalized testis morphological changes, insulin resistance, and inflammation. Conclusion: The use of Dill normalized oxidative stress, inflammation, and insulin resistance in diabetic rats that correlated with sperm profile and testis histological changes. The treatment of diabetic rat models with Dill did not show harmful effects on sperm profiles.

scholarly journals Icariin Prevents Diabetes-Induced Bone Loss in Rats by Reducing Blood Glucose and Suppressing Bone Turnover

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 1871 ◽  
Author(s):  
Shanshan Qi ◽  
Jia He ◽  
Hongxing Zheng ◽  
Chen Chen ◽  
Shiqiang Lan
Keyword(s):  
Bone Mineral Density ◽  
Bone Marrow ◽  
Blood Glucose ◽  
Bone Loss ◽  
Bone Turnover ◽  
Bone Histomorphometry ◽  
Diabetic Rats ◽  
Protective Effects ◽  
Mineral Density ◽  
Diabetic Osteoporosis

Diabetic Osteoporosis (DOP) is a common metabolic bone disease, characterized by decreased bone mineral density (BMD) and destruction of bone microstructure. It has been reported that icariin is beneficial for estrogen deficiency-induced osteoporosis, and alcohol-induced osteoporosis; whether icariin has protective effects on diabetes-induced osteoporosis has not been reported. In this study, a rat model of diabetic osteoporosis was established by streptozotocin injection, the bone protective effects and potential mechanism of icariin on diabetes-induced bone loss was observed. Thirty 8-week-old female Sprague Dawley rats were divided into control group (vehicle treatment), T1DM (diabetic) group and T1DM-icariin (ICA) group (diabetic rats treated with icariin), 10 rats in each group. The bone histomorphometry parameters, bone mineral density (BMD), serum bone turnover markers, and bone marrow adipogenesis were analyzed after 8 weeks of icariin administration. The results showed consumption of icariin at a doses of 100 mg kg−1 decreased blood glucose, and increased the BMD of diabetic rats. Icariin effectively decreased serum bone turnover marker levels, including CTX-1, ALP, TRACP 5b, osteocalcin, and PINP. Meanwhile, the bone histomorphometry parameters, the number of osteoclasts per bone perimeter were turned to be normal level, and the icariin treatment suppressed bone marrow adipogenesis. The runt-related transcription factor 2 (RUNX 2), as well as the osteoprotegerin (OPG)/receptor activator of nuclear factor-κ B ligand (RANKL) ratio in serum and bone tissues were increased significantly after icariin treatment in diabetic rats. All of the above indicate that oral administration of icariin can prevent diabetic osteoporosis; the effect is mainly related to its ability to reduce blood glucose, inhibit bone turnover and bone marrow adipogenesis, as well as up-regulate bone RUNX 2, and OPG expression.

scholarly journals Effects of Dexmedetomidine Postconditioning on Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Role of the PI3K/Akt-Dependent Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xiangyang Cheng ◽  
Jing Hu ◽  
Ya Wang ◽  
Hongwei Ye ◽  
Xiaohong Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mrna Level ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Protective Effects ◽  
Sod Activity ◽  
Group I

Objective. The present study was designed to determine whether dexmedetomidine (DEX) exerts cardioprotection against myocardial I/R injury in diabetic hearts and the mechanisms involved. Methods. A total of 30 diabetic rats induced by high-glucose-fat diet and streptozotocin (STZ) were randomly assigned to five groups: diabetic sham-operated group (DM-S), diabetic I/R group (DM-I/R), diabetic DEX group (DM-D), diabetic DEX + Wort group (DM-DW), and diabetic Wort group (DM-W). Another 12 age-matched male normal SD rats were randomly divided into two groups: sham-operated group (S) and I/R group (I/R). All rats were subjected to 30 min myocardial ischemia followed by 120 min reperfusion except sham groups. Plasmas were collected to measure the malondialdehyde (MDA), creatine kinase isoenzymes (CK-MB), and lactate dehydrogenase (LDH) levels and superoxide dismutase (SOD) activity at the end of reperfusion. Pathologic changes in myocardial tissues were observed by H-E staining. The total and phosphorylated form of Akt and GSK-3β protein expressions were measured by western blot. The ratio of Bcl-2/Bax at mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR). Results. DEX significantly reduced plasma CK-MB, MDA concentration, and LDH level and increased SOD activity caused by I/R. The phosphorylation of Akt and GSK-3β was increased, Bcl-2 mRNA and the Bcl-2/Bax ratio was increased, and Bax mRNA was decreased in the DEX group as compared to the I/R group, while posttreatment with Wort attenuated the effects induced by DEX. Conclusion. The results of this study suggest that DEX postconditioning may increase the phosphorylation of GSK-3β by activating the PI3K/Akt signaling pathway and may inhibit apoptosis and oxidative stress of the myocardium, thus exerting protective effects in diabetic rat hearts suffering from I/R injury.

scholarly journals Bone Metabolic Biomarkers-Based Diagnosis of Osteoporosis Caused by Diabetes Mellitus using Support Vector Machine

2020 ◽  
Author(s):  
Chuan Wang ◽  
Taomin Zhang ◽  
Xuan Liu ◽  
Lei Miao ◽  
Deyu Zhou ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bone Metabolism ◽  
Classification Performance ◽  
Support Vector ◽  
Mineral Density ◽  
Daily Monitoring ◽  
Diabetic Osteoporosis ◽  
Biochemical Indices ◽  
Metabolic Biomarkers

Abstract Background: Diabetes has significant effects on bone metabolism. Both type 1 and type 2 diabetes can cause osteoporotic fracture. However, it remains challenging to diagnose osteoporosis in type 2 diabetes by bone mineral density which lacks regular changes. Seen another way, osteoporosis can be ascribed to the imbalance of bone metabolism, which is closely related to diabetes as well. Method: Here, to assist clinicians in diagnosing osteoporosis in type 2 diabetes, an efficient and simple SVM model was established based on different combinations of biochemical indices, including bone turnover makers, calcium and phosphorus, etc. The classification performance was measured using several evaluations. Results: The predicting accuracy rate of final model is above 88%, with feature combination of Sex, Age, BMI, TP1NP and OSTEOC. Conclusion: Experimental results show that the model has come to an anticipant result for early detection and daily monitoring on type 2 diabetic osteoporosis.

Oxidative stress and altered prostanoid production in the placenta of streptozotocin-induced diabetic rats

2002 ◽  
Vol 14 (2) ◽  
pp. 117 ◽  
Author(s):  
Verónica White ◽  
Alicia Jawerbaum ◽  
Débora Sinner ◽  
Carolina Pustovrh ◽  
Evangelina Capobianco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Incubation Medium ◽  
Late Pregnancy ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Sod Activity ◽  
Pregnant Rats ◽  
Prostanoid Production ◽  
And Function ◽  
Diabetic Placenta

The oxidative stress in placental tissues during late pregnancy, as well as the relationship between reactive oxygen species (ROS) and the arachidonic acid (AA) pathway was evaluated in a neonatal streptozotocin (STZ)-induced diabetic rat model. Lipoperoxide levels are increased in diabetic tissues compared with control tissues (P<0.001) and they seem to increase throughout the development of gestation both in control (P<0.05) and STZ-induced diabetic (P<0.001) rats. Superoxide dismutase (SOD) activity is not modified on different days of pregnancy, but enzymatic activity is lower in diabetic tissues than in control tissues (P<0.01). Labour is preceded by an increase in placental 14C-prostaglandin conversion from 14C-AA in control and diabetic animals (P<0.05) and the thromboxane B2 (TXB2)/6-keto-prostaglandin F1α (PGF1α) ratio is higher in diabetic placental tissues than in controls. The addition of SOD and glutathione to the incubation medium does not modify prostanoid levels in control rats, but does decrease the AA conversion to PGF2α, PGE2 and TXB2 (P<0.05) in diabetic placenta. Superoxide radical generation (hypoxanthine/xanthine oxidase or hydrogen peroxide added to the incubation medium) produces a decrease in 6-keto-PGF1α (P<0.05) in control and diabetic tissues, whereas PGF2α, PGE2 and TXB2 levels, and PGF2α and TXB2 production are increased in control and diabetic animals respectively (P<0.05). Diabetic pregnant rats supplemented with a diet containing 400 mg day-1of α-tocopherol (vitamin E) have diminished placental PGF2α and TXB2 production and lipoperoxide levels. The results show a higher TXB2 and a decreased 6-keto-PGF1α placental production that may be linked to increased oxidative stress and to a reduced antioxidant capacity in STZ-induced diabetic rats. These imbalances, probably involved in abnormal placental structure and function, may potentially be corrected with dietary supplementation of α-tocopherol in diabetic pregnancies.

Betaine Alleviates Cognitive Deficits in Diabetic Rats via PI3K/Akt Signaling Pathway Regulation

2020 ◽  
Vol 49 (3) ◽  
pp. 270-278 ◽  
Author(s):  
Bingqing Huang ◽  
Xiaoli Hu ◽  
Jie Hu ◽  
Zhenfei Chen ◽  
Hao Zhao
Keyword(s):  
Signaling Pathway ◽  
Cognitive Deficits ◽  
Akt Signaling ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Akt Signaling Pathway ◽  
Sod Activity ◽  
Akt Activation ◽  
Tnf Α ◽  
Pathway Regulation

<b><i>Background:</i></b> Diabetes mellitus is a metabolic disease which also causes cognitive deficits. Betaine (N,N,N-trimethylglycine), also known as trimethylglycine, has been shown to ameliorate diabetic symptoms in diabetic animals and improve cognitive ability in Alzheimer disease (AD) animals. However, the effects of betaine on cognitive deficits in diabetic animals have not been described yet. Therefore, in the current study, the effects of betaine on cognition in diabetic rats were evaluated. <b><i>Methods:</i></b> We established a diabetic rat model by injecting streptozotocin (STZ) into rats and administrated betaine to these diabetic rats. We monitored the metabolism index, and glucose and insulin levels in blood and cerebrospinal fluid. We measured inflammatory cytokine levels, including TNF-α, IL-1β, and IL-6, in serum and hippocampus. We also monitored oxidative stress in the hippocampus by measuring malondialdehyde (MDA) level and superoxide dismutase (SOD) activity. We measured the learning and memory ability of diabetic rats using the Morris water and Y maze tests and tested the phosphatidylinositol 3-kinase (PI3K)/Akt activation and p-mTOR level in the hippocampus. <b><i>Results:</i></b> Betaine improved glucose metabolism and suppressed the production of inflammatory cytokines, including TNF-α, IL-1β, and IL-6. Also, betaine decreased MDA concentration and increased SOD activity in the hippocampus of diabetic rats. Betaine ameliorated cognitive deficits in diabetic rats, and it promoted PI3K expression and Akt activation and decreased p-mTOR expression. <b><i>Conclusion:</i></b> Betaine alleviates cognitive deficits in STZ-induced diabetic rats via regulating the PI3K/Akt signaling pathway.

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