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Background: Morin is a flavanoid which exhibits potent antioxidant activity in various oxidative stress related diseases. The current study was attempted to scrutinize the preclinical bio-efficacy of morin on focal ischemia., Methods: The animal model of focal cerebral ischemic injury was done by midbrain carotid artery occlusion (MCAO) method, followed by Morin (30mg/kg) administration for seven days., Results: The outcome of the study showed that treatment with morin displayed positive effects in reducing the focal cerebral ischemia. This effect was evident with the improvements in neurological deficits, reduction in MDA content and elevation of antioxidant levels (SOD, GSH and Gpx). Furthermore, protein expression of Bax and caspase-3 were effectively down-regulated, whilst the expression of Bcl-2 was significantly elevated. On the other hand, the mRNA expression of proinflammatory cytokines was significantly reduced in focal cerebral ischemic rats upon morin intervention., Conclusion: Thus, the beneficial effects of morin on cerebral ischemia assault may result from the reduction of oxidative stress, inhibition of apoptosis and inflammation. The neuroprotective effects of morin supplement may serve as potent adjuvant in the amelioration of ischemic stroke.

In this study, we examined the cardiovascular protective effects of IL-1ra-Fc-IL-18BP on experimental myocardial infarction in a rat model. An animal model of myocardial infarction (MI) was induced by permanent ligation of the left anterior descending coronary artery (LAD) in SD rats. After surgery sixty male rats and sixty female rats were randomly divided into groups as followed: sham group, MI group, IL-1ra-Fc-IL-18BP 50,100, 200 mg/kg treatment groups, and verapamil 5 mg/kg treatment group. IL-1 ra-Fc-IL-18BP and verapamil were administered to the animals immediately after operation by intravenous injection. Treatment with IL-1ra-Fc-IL-18BP (50, 100 and 200 mg/kg) could remarkably decrease infarct size from 24.82% to 13.43% (p < 0.05), and decrease the activities of serum aspartate aminotransferase (AST), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) compared with sham group (p < 0.05). Meanwhile, treatment with IL-1ra-Fc-IL-18BP (200 mg/kg) could significantly increase the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), but decreased the content of malondiadehyde (MDA) in serum (p < 0.05). Furthermore, IL-1ra-Fc-IL-18BP marablely reduced the content of calcium (Ca2+) in serum (p < 0.05), and also decreased the levels of serum interleukin-1β (IL-1β), tumor necrosis factor (TNF-α) (p < 0.05). Histopathological results demonstrated the same protective effect of IL-1ra-Fc-IL-18BP All these results above indicated that IL-1ra-Fc-IL-18BP has protective effects in myocardial infarction, improves free radicals metabolism, ameliorates myocardial calcium overload and inhibits the release of inflammatory cytokines.

Acanthopanax senticosides B is a monomer of Acanthopanax senticosus saponins. Previous reports showed that Acanthopanax senticosus saponins exhibit antioxidant action and cardiac protection. However, whether Acanthopanax senticosides B has cardiac protection remains unknown. In this study, we investigated the effect of Acanthopanax senticosides B on oxidative damage induced by hydrogen peroxide (H(2)O(2)) of cardiomyocytes. As revealed from the results, when the cardiomyocytes were exposed to H(2)O(2) for designed time and concentration, the percentage of survival cells was down significantly, the activity of lactate dehydrogenase (LDH) and the content of cellular malondialdehyde (MDA) were increased markedly. These results indicated that the cells were subjected to oxidative damage. Treatment with Acanthopanax senticosides B prior to H(2)O(2) (100 microM) exposure can increase cell viability significantly, lessen H(2)O(2)-induced cardiomyocyte morphological change, and inhibit augmentation of LDH activity in culture media and cellular MDA content markedly. Our results demonstrated that Acanthopanax senticosides B (400 microg/ml and 200 microg/ml) can protect cells against oxidative injury of H(2)O(2) (100 microM). Furthermore, the activities of superoxide dismutase (SOD), glutathione peroxidase, catalase and the content of reduced glutathione (GSH) of cardiomyocytes were also raised by Acanthopanax senticosides B. Taken together, the study implicated that Acanthopanax senticosides B protects cardiomyocytes against oxidative-stress injury induced by H(2)O(2) through reduction of lipid peroxidation and enhancement of the activity of antioxidant defense., (Copyright (c) 2009 Elsevier B.V. All rights reserved.)

Objective: To investigate the effect of Acanthopanax senticosus saponins (ASS) on oxidative damage induced by hydrogen peroxide (H2O2 ) in cardiomyocytes., Method: The cardiomyocytes were induced to oxidative damaged by exposed to H2O2. We evaluated the level of oxidative injury through morphology change, the survival rate, the activity of lactate dehydrogenase (LDH) and the content of cellular malondialdehyde (MDA). The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the content of reductive glutathione (GSH) of cardiomyocytes were also determined., Result: When the cardiomyocytes were exposed to H2O, (50, 100, 200 micromol x L(-1)) for deigned time, the percentage of survival cells was down significantly (P < 0.01 or P < 0.001), and the activity of LDH and the content of MDA were increased markedly (P < 0.05, P < 0.01 or P < 0.001). These results show that the cells were subjected to oxidative damage. Treatment with ASS (600 mg x L(-1)) prior to H2O2 exposure could increase cell viability significantly, lessen cardiomyocyte morphological damaged change, and decrease LDH activity (1687.40 +/- 97.51) U x mL(-1) in media and cellular MDA content (16.50 +/- 2.66) nmol x mg(-1) markedly (P < 0.01 and P < 0.05). Furthermore, the activities of SOD (89.55 +/- 6.93) U x mg(-1), GSH-Px (845.87 +/- 63.76) mU x mg(-1), CAT (93.07 +/- 10.40) U x mg(-1) and the content of GSH (8.91 +/- 1.06) micromol x mg(-1) of cardiomyocytes were also raised by 600 mg x L(-1) l ASS (P < 0.05)., Conclusion: Taken together, the study implicate that ASS protects cardiomyocytes against oxidative-stress injury induced by H2O2 through reduction of lipid peroxidation and enhancement of the activity of antioxidant defense.

Carbon tetrachloride (CCl4)-induced lipid peroxidation associated with hepatic oxidative stress and cell death is an important mechanism of acute liver injury (ALI). Ginsenoside Rd is considered an active ingredient of ginseng. Evidence suggests that ginsenoside Rd may improve ischaemic stroke, nerve damage, cancer and other diseases involving apoptosis, inflammation, oxidative stress, mitochondrial injury and autophagy. However, the effects of ginsenoside Rd on CCl4-induced ALI and its underlying mechanisms are still unclear. In this study, 0.25% CCl4 was injected intraperitoneally in mice to establish a CCl4-induced ALI model. In the Rd treatment group, Rd (10, 20 mg/kg) doses were injected intraperitoneally 1 h before and 23 h after CCl4 administration. Ferroptosis inducer imidazole ketone erastin (IKE) was injected intraperitoneally 4 h before CCl4 administration to explore the mechanism. The blood and liver were collected 24 h after CCl4 administration to investigate the effect and mechanism of ginsenoside Rd on CCl4-induced ALI. Our results showed that ginsenoside Rd inhibited CCl4-induced ALI in mice. Ginsenoside Rd also downregulated CCl4-induced serum and liver iron, 4-hydroxynonenal, and 8-hydroxy-2 deoxyguanosine levels. Furthermore, it upregulated glutathione and glutathione peroxidase 4 levels. In addition, ginsenoside Rd downregulated the expression of cGAS and STING. Subsequently, the ferroptosis inducer imidazole ketone erastin significantly reversed the hepatoprotective effect and influence of ginsenoside Rd with regard to the indicators mentioned above. Our study confirmed that ginsenoside Rd ameliorated CCl4-induced ALI in mice, which was related to the reduction of ferroptosis. Simultaneously, the ginsenoside Rd-mediated inhibition of the cGAS/STING pathway contributed to its antiferroptosis effect. In conclusion, our results suggested that ginsenoside Rd inhibited ferroptosis via the cGAS/STING pathway, thereby protecting mice from CCl4-induced ALI. These results suggested ginsenoside Rd may be used as a potential intervention treatment against CCl4-induced ALI. [ABSTRACT FROM AUTHOR]

In the present study, we aim to evaluate the potential neuroprotective effect and the underlying mechanism of Kaempferide-7-O-(4″-O-acetylrhamnosyl)-3-O-rutinoside (A-F-B) against cerebral I/R injury. Adult male rats were pretreated with A-F-B by intragastric administration once a day for 3 days. One hour after the third day administration, animals were subjected to 2 h of transient middle cerebral artery occlusion (MCAO) followed by 24 h of reperfusion. Neurological deficit, infarct volume, histopathological changes, oxidative stress-related biochemical parameters, neuronal apoptosis, apoptosis-related proteins and the expression of pro-inflammator cytokines genes were measured. A-F-B significantly decreased neurological and histological deficits, reduced the infarct volume, and decreased neuroapoptosis. Meanwhile, A-F-B inhibited the expression of Bax, cleaved caspase-3, cleaved caspase-9, and promoted Bcl-2 expression. In addition, the expression of pro-inflammator cytokines, including phospho-NF-kBp65, interleukin-1β, interleukin-6, tumor necrosis factor-α, intercellular adhesion molecule-1, cyclooxygenase-2 and inducible nitric oxide synthase, were also suppressed by A-F-B pretreatment. Furthermore, pretreatment with A-F-B could significantly increase the activities of superoxide dismutase, glutathione peroxidase, but decrease the content of malondiadehyde in blood serum. These results suggest that A-F-B has the neuroprotective effect in ischemic stroke by suppressing neuroinflammation, reactive oxygen species and neuroapoptosis. [ABSTRACT FROM AUTHOR]

• TMFP can protect diabetic cardiomyopathy in diabetic rat. • TMFP attenuated oxidative stress by increasing Nrf2 and HO-1 gene expression. • TMFP inhibited inflammation by decreasing cytokines. • TMFP alleviated apoptosis by mitochondrial pathway. The leaves of Murraya paniculata (L.) Jack were used as spices in China for many years. Flavonoids are the main components of it. However, no study has determined whether the total flavonoids of Murraya paniculata (L.) Jack (TFMP) has preventive effects on diabetic cardiomyopathy (DCM).The present study investigated the effect of TFMP on DCM. STZ was administered along with a high-fat diet to induce diabetes in rats. Parallel experiments were performed using H9c2 cells exposed to high glucose. Diabetic rats showed serious histological changes and increased levels of cardiac function markers. The markers of ROS, inflammation and apoptosis were also increased significantly, but the antioxidant defenses were decreased. Treatment with TFMP alleviated histological alteration in the myocardium. TFMP suppressed oxidative stress, inflammation and apoptosis. Our results demonstrate that the protective of TFMP on DCM is associated with increasing Nrf2 and HO-1 gene expression and inhibiting oxidative stress, inflammation and apoptosis. [ABSTRACT FROM AUTHOR]