Effect of polysaccharides extract of rhizoma atractylodis macrocephalae on thymus, spleen and cardiac indexes, caspase-3 activity ratio, Smac/DIABLO and HtrA2/Omi protein and mRNA expression levels in aged rats

Guo, Ling; Sun, Yong; Wang, Ai Hong; Xu, Chong; Zhang, Meng Yuan

doi:10.1007/s11033-012-1677-x

Cited by 25 publications

(18 citation statements)

References 24 publications

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“…Our and other’s previous studies showed the expression of Omi/HtrA2 is increased in the aging heart, which promotes cardiomyocyte apoptosis via degradation of XIAP and plays a causative role in enhanced post-ischemic injury in the aging heart1017. Here, we confirmed these findings using a transgenic model of mitochondrial Omi/HtrA2 overexpression that mimicked the conditions of an aged heart.…”

Section: Discussionsupporting

confidence: 86%

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction

Wang

Yuan

Liu

et al. 2016

Sci Rep

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Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling. Transiently or stably overexpression of mitochondria Omi/HtrA2 in H9C2 cells enhance apoptosis as evidenced by elevated caspase-3, -9 activity and TUNEL staining, which was completely blocked by Ucf-101, a specific Omi/HtrA2 inhibitor. Mechanistic studies revealed mitochondrial Omi/HtrA2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Ucf-101. Additionally, transfected cells overexpressing mitochondrial Omi/HtrA2 were more sensitive to hypoxia and reoxygenation (H/R) induced apoptosis. Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked translocation of Omi/HtrA2 from mitochondrial to cytoplasm, and protected transfected cells incompletely against H/R-induced caspase-3 activation. We report in vitro and in vivo overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. Thus, strategies to directly inhibit Omi/HtrA2 or its cytosolic translocation from mitochondria may protect against heart injury.

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Section: Discussionsupporting

confidence: 86%

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction

Wang

Yuan

Liu

et al. 2016

Sci Rep

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“…A recent study has reported that the polysaccharides extract of Atractylodes macrocephala enhanced immunity and improved heart function in aged rats (Guo et al, 2012). However, little is known regarding the role of Atractylodes macrocephalaon polysaccharides (AMP) in macrophage activation.…”

Section: Introductionmentioning

confidence: 99%

Macrophage activation by polysaccharides fromAtractylodes macrocephalaKoidz through the nuclear factor-κB pathway

Chen

Zheng

2014

Pharmaceutical Biology

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Context: Atractylodes macrocephala Koidz is a traditional herb. Atractylodes macrocephalaon polysaccharides (AMP) have been found to enhance immunity and improve heart function. However, the mechanisms of the immunomodulatory effect have not been investigated. Objective: We examined whether AMP activated macrophages and explored the mechanisms of activation. Materials and methods: AMP was prepared and evaluated its immunomodulatory activity (25, 50, 100, and 200 lg/mL) by detecting the phagocytosis and the production of tumor necrosis factor-a (TNF-a), IFN-c, and nitric oxide (NO) in RAW264.7 macrophages. Furthermore, the role of nuclear factor-kB (NF-kB) pathway was examined in regulating TNF-a and NO production. Results: The phagocytosis of macrophages was enhanced by AMP in a dose-dependent manner and the maximal phagocytosis of macrophages occurred at concentrations of 100 and 200 lg/mL. NO, TNF-a, and IFN-c release was also found to be dose dependent by increasing concentrations of AMP and reached the peak at a concentration of 200 lg/mL. In addition, AMP induced inhibitor kappaB (IkB) degradation and the activation of NF-kB by p65 nuclear translocation, and then the activation of NF-kB in nucleus peaked at a concentration of 200 lg/ mL. Besides, NF-kB-specific inhibitor pyrrolidine dithiocarbamate (PDTC) decreased AMP-induced NO and TNF-a production. Discussion and conclusion: These data suggest that AMP may modulate macrophage activities by stimulating NF-kB or activating NF-kB-dependent mechanisms.

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“…Cortex Cinnamomi has been found to improve renal function effectively in mice 36. Furthermore, the bioactive components or extracts of the Atractylodis macrocephalae rhizome have been reported to enhance immunity in aged rats 37. In summary, these reports indicate that Wuling San might have diuretic efficacy and renal protective effects by enhancing kidney function and inhibiting stress response.…”

Section: Discussionmentioning

confidence: 93%

Efficacy and safety of Wuling San for treatment of breast-cancer-related upper extremity lymphoedema: study protocol for a pilot trial

et al. 2016

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IntroductionBreast-cancer-related upper extremity lymphoedema (BCUL), a common complication of mastectomy, can cause physical discomfort, psychological distress, cosmetic defects, functional disability and chronic recurrent erysipelas in the affected arm(s). It is a challenge to physicians involved in the management of these patients. Wuling San, a classic prescription in Traditional Chinese Medicine used in treating oedema for thousands of years, is reported by many Chinese journals to perform well in BCUL. Therefore, the aim of this study is to verify its efficacy and evaluate its safety using rigorous methodological designs in patients with BCUL.Methods and analysisTo verify the efficacy and assess the safety of Wuling San over a placebo, this double-blind, randomised, placebo-controlled, multicentre trial will be carried out in three hospitals. A total of 200 eligible patients with BCUL will be randomly allocated, in a ratio of 1:1, to either the experimental medicine group or the placebo group. The primary outcome measure will be the proportion of absolute reduced limb volume, as measured by perometry. The second outcome measure will be the number of participants with adverse events. The assessment will be carried out at the following time points: before enrolment (baseline) and 2, 4, 6 and 8 weeks after treatment.Ethics and disseminationThis trial will be conducted in accordance with the Declaration of Helsinki and supervised by the institutional review board of the Fourth Affiliated Hospital of Guangxi Medical University (approval number PJK2016088). All patients will receive information about the trial in verbal and written forms and will give informed consent before enrolment. This trial will help to demonstrate whether Wuling San is effective in the treatment of patients with BCUL. The results will be published in peer-reviewed journals or disseminated through conference presentations.Trial registration numberNCT02726477; Pre-results.

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Effect of polysaccharides extract of rhizoma atractylodis macrocephalae on thymus, spleen and cardiac indexes, caspase-3 activity ratio, Smac/DIABLO and HtrA2/Omi protein and mRNA expression levels in aged rats

Cited by 25 publications

References 24 publications

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction

Macrophage activation by polysaccharides fromAtractylodes macrocephalaKoidz through the nuclear factor-κB pathway

Efficacy and safety of Wuling San for treatment of breast-cancer-related upper extremity lymphoedema: study protocol for a pilot trial

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