Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea(FOE) has gastroprotective properties. The aim of this...Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea(FOE) has gastroprotective properties. The aim of this study was to investigate the gastroprotective activity of FOE on water immersion restrained stress(WIRS)-induced gastric mucosal injury in a rat model and elucidate the possible molecular mechanisms involved.Methods: A rat stress ulcer model was established in this study using WIRS. After rats were treated with FOE orally for 7 d, the effect of FOE treatment was analyzed by hematoxylin and eosin(H&E) staining, and the changes of inflammatory factors, oxidative stress factors, and gastric-specific regulatory factors and pepsin in the blood and gastric tissues of rats were examined by ELISA assay. Molecular mechanism of FOE was investigated by immunohistochemical assay and Western blot.Results: Compared with the WIRS group, FOE could diminish both the macroscopic and microscopic pathological morphology of gastric mucosa. FOE significantly preserved the antioxidants glutathione peroxidase(GSH-PX), superoxide dismutase(SOD) and catalase(CAT) contents;anti-inflammatory cytokines interleukin-10(IL-10) and prostaglandin E2(PGE2) levels as well as regulatory factors tumor necrosis factor-a(TGF-a) and somatostatin(SS) contents, while decreasing malondialdehyde(MDA), nitric oxide synthase(i NOS), tumor necrosis factor(TNF-a), interleukin-1β(IL-1β), interleukin-6(IL-6), gastrin(GAS)and endothelin(ET) levels. Moreover, FOE distinctly upregulated the expression of Nrf2, HO-1, Bcl2 and proliferating cell nuclear antigen(PCNA). In addition, FOE activated the expression of p-EGFR and downregulated the expression of NF-ΚB, Bax, Cleaved-caspase-3, Cyto-C and Cleaved-PARP1, thus promoting gastric mucosal cell survival.Conclusion: The current work demonstrated that FOE exerted a gastroprotective activity against gastric mucosal injury induced by WIRS. The underlying mechanism might be associated with the improvement展开更多
Luteolin （3＇,4＇,5,7-tetrahydroxyflavone） has powerful anti-apoptotic and antioxidant properties. This study aimed to investigate the effects of luteolin on hyperglycemia-mediated apoptosis in the hippocampi of rat...Luteolin （3＇,4＇,5,7-tetrahydroxyflavone） has powerful anti-apoptotic and antioxidant properties. This study aimed to investigate the effects of luteolin on hyperglycemia-mediated apoptosis in the hippocampi of rats with streptozotocin-induced diabetic encephalopathy after injection into the tail veins, and the molecular mechanisms involved. Biochemistry and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling detection results showed that luteolin treatment （given twice daily for 15 days） significantly inhibited hyperglycemia-mediated apoptosis, decreased malondialdehyde levels and increased glutathione levels in the hippocampi of streptozotocin- induced diabetic rats. Western blot analysis revealed that luteolin also inhibited the expression of apoptosis-related factors and cytochrome c release from mitochondria. Luteolin also improved the learning and memory abiJities of rats with diabetic encephalopathy in a water maze test. Further western blot analysis revealed that luteolin treatment facilitated neuronal cell survival through activation of the phosphatidylinositol 3-kinase/Akt signaling pathway, an extracellular signal pathway involved in the suppression of cell apoptosis and promotion of cell survival. These experimental findings indicate that luteolin can inhibit apoptosis of hippocampal nerve cells in rats with diabetic encephalopathy, and that this effect is mediated by an indirect antioxidative effect, the inhibition of activation of apoptosis-related factors and the activation of phosphatidylinositol 3-kinase/Akt signal pathway.展开更多
3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein（an active ingredient of the kudzu vine root）. It has been shown to have a protective effect on cerebral ischemia/reperfus...3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein（an active ingredient of the kudzu vine root）. It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3′-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3′-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels. 3′-Daidzein sulfonate sodium improved the structural integrity of the blood-brain barrier and reduced blood-brain barrier permeability. These findings confirmed that 3′-daidzein sulfonate sodium has a protective effect on mitochondrial functions after cerebral ischemia/reperfusion injury, improves brain energy metabolism, and provides protection against blood-brain barrier damage.展开更多
Objective:To explore the expression of Nrf2/ARE pathway in hindbrain tissue after the traumatic brain injury（TBI） and its anli-oxidative stress effect in the secondary nerve injury.Methods: The mice with Nrf2 gene k...Objective:To explore the expression of Nrf2/ARE pathway in hindbrain tissue after the traumatic brain injury（TBI） and its anli-oxidative stress effect in the secondary nerve injury.Methods: The mice with Nrf2 gene knockout were used for the establishment of brain injury model.The experimental animals were divided into four groups:(Nrf2<sup>+/+</sup>) sham-operation group,(Nrf2<sup>+/+</sup>) brain injury group,（Nrf2T） sham-operation group and(Nrf2<sup>-/-</sup>) brain injury group.The specimen 24 h after cerebral trauma was selected.Then RT-PCR method was adopted to detect the expression of Nrf2 mRNA in brain;Western blotting method was adopted to detect the levels of Nrf2,HO-1 and NQO1 proteins in brain;EUSA method was adopted to detect the oxidative stress indicators: protein carbonyls,4-hydroxy-2-nonenal（4-HNE） and 8-hydroxy-2’-deoxyguanosine（8-OHdG）. ResuHs:The Nrf2 mRNA and protein of Nrf2<sup>-/-</sup> mice were not expressed,and the diflerence of the relative amount of Nrf2 mRNA between Nrf2<sup>+/+</sup> TBI group and Nrf2<sup>+/+</sup> sham-operation group was not statistically significant（P】0.05）;the level of Nrf2 protein in Nrf2<sup>+/+</sup> TBI group increased significantly compared with the Nrf2<sup>+/+</sup> sham-operation group（P【0.01）;in the sham-operation groups,the levels of HO-1 and NQO1 proteins of Nrf2<sup>-/-</sup> mice decreased obviously compared with the Nrf2<sup>+/+</sup> mice（P【0.01）;after brain injury,the levels of HO-1 and NQO1 proteins of Nrf2<sup>+/+</sup> mice increased obviously compared with the corresponding sham-operation group（P【0.01）;the levels of HO-1 and NQOl proteins of Nrf2<sup>-/-</sup> mice in TBI group had no obvious change compared with the corresponding sham-operation group（P】0.05）;there was only a little amount of expression of protein carbonyls,4-HNE and 8-OHdG proteins in brain tissues in the Nrf2<sup>-/+</sup> and Nrf2<sup>-/-</sup> shamoperation groups,and the difference was not statistically significant（P&展开更多
Recent evidence exists that enoxaparin can reduce brain injury because of its anticoagulant activity. To investigate the potential therapeutic effect of enoxaparin on cold-induced traumatic brain injury, at 20 minutes...Recent evidence exists that enoxaparin can reduce brain injury because of its anticoagulant activity. To investigate the potential therapeutic effect of enoxaparin on cold-induced traumatic brain injury, at 20 minutes after modeling, male BALB/c mouse models of cold-induced traumatic brain injury were intraperitoneally administered 3 and 10 mg/kg enoxaparin or isotonic saline solution. Twenty-four hours later, enoxaparin at 10 mg/kg greatly reduced infarct volume, decreased cell apoptosis in the cortex and obviously increased serum level of total antioxidant status. By contrast, administration of enoxaparin at 3 mg/kg did not lead to these changes. These findings suggest that enoxaparin exhibits neuroprotective effect on cold-induced traumatic brain injury in a dose-dependent manner.展开更多
基金supported by the National Natural Science Foundation of China(No.81673693)the National Key R&D Program of China(No.2017YFD0201402)for financial support.
文摘Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea(FOE) has gastroprotective properties. The aim of this study was to investigate the gastroprotective activity of FOE on water immersion restrained stress(WIRS)-induced gastric mucosal injury in a rat model and elucidate the possible molecular mechanisms involved.Methods: A rat stress ulcer model was established in this study using WIRS. After rats were treated with FOE orally for 7 d, the effect of FOE treatment was analyzed by hematoxylin and eosin(H&E) staining, and the changes of inflammatory factors, oxidative stress factors, and gastric-specific regulatory factors and pepsin in the blood and gastric tissues of rats were examined by ELISA assay. Molecular mechanism of FOE was investigated by immunohistochemical assay and Western blot.Results: Compared with the WIRS group, FOE could diminish both the macroscopic and microscopic pathological morphology of gastric mucosa. FOE significantly preserved the antioxidants glutathione peroxidase(GSH-PX), superoxide dismutase(SOD) and catalase(CAT) contents;anti-inflammatory cytokines interleukin-10(IL-10) and prostaglandin E2(PGE2) levels as well as regulatory factors tumor necrosis factor-a(TGF-a) and somatostatin(SS) contents, while decreasing malondialdehyde(MDA), nitric oxide synthase(i NOS), tumor necrosis factor(TNF-a), interleukin-1β(IL-1β), interleukin-6(IL-6), gastrin(GAS)and endothelin(ET) levels. Moreover, FOE distinctly upregulated the expression of Nrf2, HO-1, Bcl2 and proliferating cell nuclear antigen(PCNA). In addition, FOE activated the expression of p-EGFR and downregulated the expression of NF-ΚB, Bax, Cleaved-caspase-3, Cyto-C and Cleaved-PARP1, thus promoting gastric mucosal cell survival.Conclusion: The current work demonstrated that FOE exerted a gastroprotective activity against gastric mucosal injury induced by WIRS. The underlying mechanism might be associated with the improvement
文摘Luteolin （3＇,4＇,5,7-tetrahydroxyflavone） has powerful anti-apoptotic and antioxidant properties. This study aimed to investigate the effects of luteolin on hyperglycemia-mediated apoptosis in the hippocampi of rats with streptozotocin-induced diabetic encephalopathy after injection into the tail veins, and the molecular mechanisms involved. Biochemistry and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling detection results showed that luteolin treatment （given twice daily for 15 days） significantly inhibited hyperglycemia-mediated apoptosis, decreased malondialdehyde levels and increased glutathione levels in the hippocampi of streptozotocin- induced diabetic rats. Western blot analysis revealed that luteolin also inhibited the expression of apoptosis-related factors and cytochrome c release from mitochondria. Luteolin also improved the learning and memory abiJities of rats with diabetic encephalopathy in a water maze test. Further western blot analysis revealed that luteolin treatment facilitated neuronal cell survival through activation of the phosphatidylinositol 3-kinase/Akt signaling pathway, an extracellular signal pathway involved in the suppression of cell apoptosis and promotion of cell survival. These experimental findings indicate that luteolin can inhibit apoptosis of hippocampal nerve cells in rats with diabetic encephalopathy, and that this effect is mediated by an indirect antioxidative effect, the inhibition of activation of apoptosis-related factors and the activation of phosphatidylinositol 3-kinase/Akt signal pathway.
基金supported by the National Natural Science Foundation of China,No.81160399,81560583the Science and Technology Landing Project of China,No.KJLD13085the Science and Technology Project of the Education Department of Jiangxi Province of China,No.GJJ12560
文摘3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein（an active ingredient of the kudzu vine root）. It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3′-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3′-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels. 3′-Daidzein sulfonate sodium improved the structural integrity of the blood-brain barrier and reduced blood-brain barrier permeability. These findings confirmed that 3′-daidzein sulfonate sodium has a protective effect on mitochondrial functions after cerebral ischemia/reperfusion injury, improves brain energy metabolism, and provides protection against blood-brain barrier damage.
文摘Objective:To explore the expression of Nrf2/ARE pathway in hindbrain tissue after the traumatic brain injury（TBI） and its anli-oxidative stress effect in the secondary nerve injury.Methods: The mice with Nrf2 gene knockout were used for the establishment of brain injury model.The experimental animals were divided into four groups:(Nrf2<sup>+/+</sup>) sham-operation group,(Nrf2<sup>+/+</sup>) brain injury group,（Nrf2T） sham-operation group and(Nrf2<sup>-/-</sup>) brain injury group.The specimen 24 h after cerebral trauma was selected.Then RT-PCR method was adopted to detect the expression of Nrf2 mRNA in brain;Western blotting method was adopted to detect the levels of Nrf2,HO-1 and NQO1 proteins in brain;EUSA method was adopted to detect the oxidative stress indicators: protein carbonyls,4-hydroxy-2-nonenal（4-HNE） and 8-hydroxy-2’-deoxyguanosine（8-OHdG）. ResuHs:The Nrf2 mRNA and protein of Nrf2<sup>-/-</sup> mice were not expressed,and the diflerence of the relative amount of Nrf2 mRNA between Nrf2<sup>+/+</sup> TBI group and Nrf2<sup>+/+</sup> sham-operation group was not statistically significant（P】0.05）;the level of Nrf2 protein in Nrf2<sup>+/+</sup> TBI group increased significantly compared with the Nrf2<sup>+/+</sup> sham-operation group（P【0.01）;in the sham-operation groups,the levels of HO-1 and NQO1 proteins of Nrf2<sup>-/-</sup> mice decreased obviously compared with the Nrf2<sup>+/+</sup> mice（P【0.01）;after brain injury,the levels of HO-1 and NQO1 proteins of Nrf2<sup>+/+</sup> mice increased obviously compared with the corresponding sham-operation group（P【0.01）;the levels of HO-1 and NQOl proteins of Nrf2<sup>-/-</sup> mice in TBI group had no obvious change compared with the corresponding sham-operation group（P】0.05）;there was only a little amount of expression of protein carbonyls,4-HNE and 8-OHdG proteins in brain tissues in the Nrf2<sup>-/+</sup> and Nrf2<sup>-/-</sup> shamoperation groups,and the difference was not statistically significant（P&
文摘Recent evidence exists that enoxaparin can reduce brain injury because of its anticoagulant activity. To investigate the potential therapeutic effect of enoxaparin on cold-induced traumatic brain injury, at 20 minutes after modeling, male BALB/c mouse models of cold-induced traumatic brain injury were intraperitoneally administered 3 and 10 mg/kg enoxaparin or isotonic saline solution. Twenty-four hours later, enoxaparin at 10 mg/kg greatly reduced infarct volume, decreased cell apoptosis in the cortex and obviously increased serum level of total antioxidant status. By contrast, administration of enoxaparin at 3 mg/kg did not lead to these changes. These findings suggest that enoxaparin exhibits neuroprotective effect on cold-induced traumatic brain injury in a dose-dependent manner.
