scholarly journals Corrigendum: Cardioprotective Effect of Stem-Leaf Saponins From Panax notoginseng on Mice With Sleep Deprivation by Inhibiting Abnormal Autophagy Through PI3K/Akt/mTOR Pathway

2022 ◽  
Vol 8 ◽  
Author(s):  
Yin Cao ◽  
Qinglin Li ◽  
Yingbo Yang ◽  
Zunji Ke ◽  
Shengqi Chen ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Panax Notoginseng ◽  
Mtor Pathway ◽  
Cardioprotective Effect ◽  
Stem Leaf

scholarly journals Total Saponins of Panax Notoginseng Exhibit Neuroprotection by The Activation of Akt/mTOR Pathway in Vitro and in Vivo

2020 ◽  
Author(s):  
Dong-Ping Wu ◽  
Yu-Wei Pan ◽  
Hua-Feng Liang ◽  
Gen-Yun Tang ◽  
Ming Chen ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cerebral Ischemia ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Panax Notoginseng ◽  
Mtor Pathway ◽  
Dead Cell ◽  
Cerebral Ischemia Reperfusion ◽  
Underlying Mechanisms

Abstract Background: Panax notoginseng (Burkill) F.H.Chen is a traditional Chinese medicine. The present study reports the potential therapeutic effect of total saponins of Panax notoginseng (Burkill) F.H.Chen (TSPN) on ischemic stroke and investigates the underlying mechanisms. To reveal the neuroprotective effect of TSPN on cerebral ischemia-reperfusion injury and the underlying mechanisms.Methods: Oxygen-glucose deprivation/reoxygenation (OGD/R) of cultured cortical neurons was used as a model of neuronal injury. The neuroprotective effect of TSPN was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, flow cytometry and Live/Dead cell assay. The morphology of dendrites was detected by immunofluorescence. Rat middle cerebral artery occlusion (MCAO) was used as a model of cerebral ischemia-reperfusion. The neuroprotective effect of TSPN was evaluated by neurological score, tail hang test, TTC staining, and Nissl staining. Western blot analysis, immunohistochemistry or immunofluorescence was used to measure the changes in Akt/mTOR signaling pathway.Results: MTT showed that TSPN had a rescue effect on cortical neurons after OGD/R-treated. Flow cytometry and Live/Dead cell assay indicated that TSPN decreased neuronal apoptosis, and immunofluorescence showed that TSPN restored dendrite morphology of the damaged neurons. Moreover, TSPN down-regulated the expressions of cleaved-Caspase-3 and LC3B-II/LC3B-I, whereas up-regulated the levels of phosphorylated (p)- Akt and p-mTOR. In MCAO model, TSPN rescued defective neurological behavior and reduced infarct volume. Moreover, the expressions of Beclin-1 and LC3B in cerebral ischemic penumbra were down-regulated after the treatment of TSPN, whereas p-mTOR level was up-regulated.Conclusion: TSPN show neuroprotective effects against OGD/R-induced cortical neuronal damage and exhibit potential therapeutic effects on cerebral ischemia in rat MCAO model. Up-regulation of mTOR pathway and inhibition of the autophagic pathway could be the mechanisms that underlie the action of TSPN.

scholarly journals 0028 Sleep Duration Influences the Kinetics of Stress Granule Formation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A11-A12
Author(s):  
M K Dougherty ◽  
C Saul ◽  
L Carman ◽  
M D Nelson ◽  
J C Tudor
Keyword(s):  
Sleep Deprivation ◽  
Sleep Duration ◽  
Protein A ◽  
Stress Granules ◽  
Mtor Pathway ◽  
Stress Granule ◽  
Target Of Rapamycin ◽  
Granule Formation ◽  
One Way Anova

Abstract Introduction Stress granules are non-membrane bound aggregates of messenger ribonucleoproteins that are biomarkers of cellular stress. It has been shown in cells in vitro that suppression of the mammalian target of rapamycin (mTOR) pathway and its non-mammalian orthologue target of rapamycin (TOR) is associated with an increase in stress granule formation. It has also been shown that the mTOR pathway is suppressed in response to sleep deprivation in mice. Despite the possible connection via the TOR/mTOR pathway, there has not been any previous evidence linking sleep deprivation with stress granule formation. Methods Our present investigation uses the nematode Caenorhabditis elegans to model how stress granule formation and clearance are modified by sleep duration. We developed novel strains of C. elegans that model each type of sleep deprivation or enhancement and have RFP-labeled PAB-1 protein, a key component of stress granules. In addition to modifying sleep duration via genetic means, we also sleep deprived wildtype fluorescently labeled animals using mechanical disturbances. Results Animals with enhanced stress-induced sleep have stress granules that are smaller in size and cleared faster than wildtype, while sleep deprived animals have granules that are slower to clear (F11,473 = 7.752, ***p < 0.0001, one-way ANOVA). Animals that were manually deprived of stress-induced sleep were similarly slower to clear stress granules (F5,209 = 5.476 ***p < 0.0001, one-way ANOVA). Interestingly, animals genetically deprived of developmentally-timed sleep does not appear to have more stress granules in the middle of their sleep period than the sleeping wildtype stage (F2,42 = 2.659, p = 0.0729, one-way ANOVA). Conclusion This work demonstrates that the amount of sleep affects stress granule kinetics, which impacts the flow of genetic information inside cells. Support This work was supported by an R15GM122058 (NIH), John P. McNulty scholars program (SJU) and summer scholars program (SJU).

scholarly journals Cardioprotective Effect of Stem-Leaf Saponins From Panax notoginseng on Mice With Sleep Derivation by Inhibiting Abnormal Autophagy Through PI3K/Akt/mTOR Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Yin Cao ◽  
Qinglin Li ◽  
Yingbo Yang ◽  
Zunji Ke ◽  
Shengqi Chen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Myocardial Injury ◽  
Panax Notoginseng ◽  
Heart Tissue ◽  
H9c2 Cells ◽  
Mtor Signaling Pathway ◽  
Western Blotting Analysis ◽  
Stem Leaf

Sleep deprivation (SD) may lead to serious myocardial injury in cardiovascular diseases. Saponins extracted from the roots of Panax notoginseng, a traditional Chinese medicine beneficial to blood circulation and hemostasis, are the main bioactive components exerting cardiovascular protection in the treatment of heart disorders, such as arrhythmia, ischemia and reperfusion injury, and cardiac hypertrophy. This study aimed to explore the protective effect of stem-leaf saponins from Panax notoginseng (SLSP) on myocardial injury in SD mice. SD was induced by a modified multi-platform method. Cardiac morphological changes were assessed by hematoxylin and eosin (H&E) staining. Heart rate and ejection fraction were detected by specific instruments. Serum levels of atrial natriuretic peptide (ANP) and lactate dehydrogenase (LDH) were measured with biochemical kits. Transmission electron microscopy (TEM), immunofluorescent, and Western blotting analysis were used to observe the process and pathway of autophagy and apoptosis in heart tissue of SD mice. In vitro, rat H9c2 cells pretreated with rapamycin and the effect of SLSP were explored by acridine orange staining, transient transfection, flow cytometry, and Western blotting analysis. SLSP prevented myocardial injury, such as morphological damage, accumulation of autophagosomes in heart tissue, abnormal high heart rate, serum ANP, and serum LDH induced by SD. In addition, it reversed the expressions of proteins involved in the autophagy and apoptosis and activated PI3K/Akt/mTOR signaling pathway that is disturbed by SD. On H9c2 cells induced by rapamycin, SLSP could markedly resume the abnormal autophagy and apoptosis. Collectively, SLSP attenuated excessive autophagy and apoptosis in myocardial cells in heart tissue induced by SD, which might be acted through activating PI3K/Akt/mTOR signaling pathway.

scholarly journals Optimization of Flavonoids Extraction Process in Panax notoginseng Stem Leaf and a Study of Antioxidant Activity and Its Effects on Mouse Melanoma B16 Cells

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2219 ◽  
Author(s):  
Chun-Yan Dai ◽  
Peng-Fei Liu ◽  
Pei-Ran Liao ◽  
Yuan Qu ◽  
Cheng-Xiao Wang ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Free Radical ◽  
Sodium Dodecyl ◽  
Radical Scavenging ◽  
Panax Notoginseng ◽  
Extraction Process ◽  
Utilization Rate ◽  
Leaf Extracts ◽  
Ic50 Values ◽  
Stem Leaf

The Panax notoginseng (P. notoginseng) stem leaf is rich in flavonoids. However, because of a lack of research on the flavonoid extraction process and functional development of P. notoginseng stem leaf, these parts are discarded as agricultural wastes. Therefore, in this study, we intend to optimize the extraction process and develop the skin-whitening functions of P. notoginseng stem leaf extracts. The extraction process of the stem and leaf of P. notoginseng flavonoid (SLPF) is optimized based on the Box–Behnken design (BBD) and the response surface methodology (RSM). The optimum extraction conditions of the SLPF are as follows: the extraction time, the ethanol concentration, the sodium dodecyl sulfate (SDS) content and the liquid material ratio (v/w, which are 52 min, 48.7%, 1.9%, and 20:1, respectively. Under the optimal extraction conditions, the average total SLPF content is 2.10%. The antioxidant activity and anti-deposition of melanin of mouse B16 cells of P. notoginseng stem leaf extracts are studied. The results indicate that the EC50 values of reducing activity, 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging activities, the superoxide anion removal ability, and the 2,2-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS) free radical removal ability are 7.212, 2.893, 2.949, and 0.855 mg/mL, respectively. The extracts IC50 values of the tyrosinase and melanin synthesis are 0.045 and 0.046 mg/mL, respectively. Therefore, the optimal processing technology for the SLPF obtained in this study not only increases its utilization rate, but also decreases material costs. The extracts from the P. notoginseng stem leaf may be developed as food or beauty products.

scholarly journals Xuesaitong Protects Podocytes from Apoptosis in Diabetic Rats through Modulating PTEN-PDK1-Akt-mTOR Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Rui Xue ◽  
Ruonan Zhai ◽  
Ling Xie ◽  
Zening Zheng ◽  
Guihua Jian ◽  
...  
Keyword(s):  
Diabetic Kidney Disease ◽  
Morphological Changes ◽  
Panax Notoginseng ◽  
Diabetic Rats ◽  
Mtor Pathway ◽  
Phosphorylated Akt ◽  
Immunofluorescence Labelling ◽  
Stage Renal Disease ◽  
End Stage ◽  
Renal Expression

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease (ESRD), and therapeutic strategies for delaying its progression are limited. Loss of podocytes by apoptosis characterizes the early stages of DKD. To identify novel therapeutic options, we investigated the effects of Xuesaitong (XST), consisting of total saponins from Panax notoginseng, on podocyte apoptosis in streptozotocin- (STZ-) induced diabetic rats. XST (5 mg/kg·d) or Losartan (10 mg/kg·d) was given to diabetic rats for 12 weeks. Albuminuria, renal function markers, and renal histopathology morphological changes were examined. Podocyte apoptosis was determined by triple immunofluorescence labelling including a TUNEL assay, WT1, and DAPI. Renal expression of Nox4, miRNA-214, PTEN, PDK1, phosphorylated Akt, mTOR, and mTORC1 was detected. In diabetic rats, severe hyperglycaemia and albuminuria developed, and apoptotic podocytes were markedly increased in diabetic kidneys. However, XST attenuated albuminuria, mesangial expansion, podocyte apoptosis, and morphological changes of podocytes in diabetic rats. Decreased expression of PTEN, as well as increased expression of Nox4, miRNA-214, PDK1, phosphorylated Akt, mTOR, and mTORC1, was detected. These abnormalities were partially restored by XST treatment. Thus, XST ameliorated podocyte apoptosis partly through modulating the PTEN-PDK1-Akt-mTOR pathway. These novel findings might point the way to a natural therapeutic strategy for treating DKD.

scholarly journals Notoginsenoside R1 Reverses Abnormal Autophagy in Hippocampal Neurons of Mice With Sleep Deprivation Through Melatonin Receptor 1A

2021 ◽  
Vol 12 ◽  
Author(s):  
Yin Cao ◽  
Qinglin Li ◽  
An Zhou ◽  
Zunji Ke ◽  
Shengqi Chen ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Signaling Pathway ◽  
Learning And Memory ◽  
Hippocampal Neurons ◽  
Panax Notoginseng ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Melatonin Receptor ◽  
Sleep Regulation ◽  
Neural Injury

Sleep deprivation (SD) may cause serious neural injury in the central nervous system, leading to impairment of learning and memory. Melatonin receptor 1A (MTNR1A) plays an important role in the sleep regulation upon activation by melatonin. The present study aimed to investigate if notoginsenoside R1 (NGR1), an active compound isolated from Panax notoginseng, could alleviate neural injury, thus improve impaired learning and memory of SD mice, as well as to explore its underlying action mechanism through modulating MTNR1A. Our results showed that NGR1 administration improved the impaired learning and memory of SD mice. NGR1 prevented the morphological damage and the accumulation of autophagosomes in the hippocampus of SD mice. At the molecular level, NGR1 reversed the expressions of proteins involved in autophagy and apoptosis, such as beclin-1, LC3B, p62, Bcl-2, Bax, and cleaved-caspase 3. Furthermore, the effect of NGR1 was found to be closely related with the MTNR1A-mediated PI3K/Akt/mTOR signaling pathway. On HT-22 cells induced by autophagy inducer rapamycin, NGR1 markedly attenuated excessive autophagy and apoptosis, and the alleviative effect was abolished by the MTNR1A inhibitor. Taken together, NGR1 was shown to alleviate the impaired learning and memory of SD mice, and its function might be exerted through reduction of excessive autophagy and apoptosis of hippocampal neurons by regulating the MTNR1A-mediated PI3K/Akt/mTOR signaling pathway.

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