PMID: 

Respir Physiol Neurobiol. 2019 Oct ;268:103252. Epub 2019 Jul 10. PMID: 31301382

Abstract Title: 

Paeonol protects mitochondrial injury and prevents pulmonary vascular remodeling in hypoxia.

Abstract: 

Mitochondrial injury of pulmonary artery smooth muscle cells (PASMCs) is an important stage in the development of pulmonary arterial hypertension (PAH). Recent studies revealed that Paeonol exerts anti-proliferative effects on vascular smooth muscle cells. However, whether Paeonol is directly involved in mitochondrial injury related to PAH remains unknown. Here, we found that hypoxia-induced mitochondrial injury in vivo was alleviated in the presence of Paeonol. Hypoxia mediated the mitochondrial injuries in PASMCs in vitro, including decreased ATP generation, morphological alterations, mitochondrial polarization and increased reactive oxygen species production, which were suppressed by Paeonol. Our results also indicated that the expression of peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) was regulated by Paeonol. Paeonol caused significant alterations in mitochondrion-dependent apoptosis through PGC-1α in PASMCs. Taken together, these results provide the first evidence confirming the protective effect of Paeonol in mediating mitochondrial injury under hypoxia and elucidating the necessary role of PGC-1α in the effects of Paeonol in inducing PASMC apoptosis.

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PMID: 

Chem Res Toxicol. 2019 Jul 16. Epub 2019 Jul 16. PMID: 31307187

Abstract Title: 

Paeonol Reverses Adriamycin Induced Cardiac Pathological Remodeling through Notch1 Signaling Reactivation in H9c2 Cells and Adult Zebrafish Heart.

Abstract: 

Adriamycin is a commonly prescribed chemotherapeutic drug for a wide range of cancers. Adriamycin causes cardiotoxicity as an adverse effect that limits its clinical application in cancer treatment. Several mechanisms have been proposed to explain the toxicity it causes in heart cells. Disruption of inherent cardiac repair mechanism is the least understood mechanism of Adriamycin-induced cardiotoxicity. Adriamycin induces pathological remodeling in cardiac cells by promoting apoptosis, hypertrophy and fibrosis. We found that Adriamycin inhibited Notch1 in a time and dose dependent manner in H9c2 cells. We used Paeonol, a Notch1 activator and analyzed the markers of apoptosis, hypertrophy and fibrosis in H9c2 cells in vitro and in adult zebrafish heart in vivo as model system to study Adriamycin induced cardiotoxicity. Paeonol activated Notch1 signaling and expression of its downstream target genes effectively in the Adriamycin treated condition invitro and in vivo. Also we detected that Notch activation using Paeonol protected the cells from apoptosis, collagen deposition and hypertrophy response using functional assays. We conclude that Adriamycin induced cardiotoxicity by promoting the pathological cardiac remodeling through inhibition of Notch1 signaling and that the Notch1 reactivation by Paeonol protected the cells and reversed the cardiotoxicity.

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PMID: 

Biosci Biotechnol Biochem. 2019 Nov ;83(11):1992-1999. Epub 2019 Jul 31. PMID: 31362597

Abstract Title: 

Paeonol protects against hypertension in spontaneously hypertensive rats by restoring vascular endothelium.

Abstract: 

The present study focused on the effect of paeonol, one of the main components of Guizhi Fuling Pill, on blood pressure, cerebral blood flow, and vascular endothelium injury in spontaneously hypertensive rats to provide theoretical basis for the treatment of hypertension. After treatment with paeonol, the mean arterial pressure (MAP) of LSHRT and HSHRT rats decreased gradually with the prolongation of treatment time. The systolic blood flow velocity (Vs), diastolic blood flow velocity (Vd) and mean blood flow velocity (Vm) were significantly increased after paeonol treatment (

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PMID: 

Phytother Res. 2019 Nov ;33(11):2971-2978. Epub 2019 Aug 12. PMID: 31407455

Abstract Title: 

Paeonol ameliorates monosodium urate-induced arthritis in rats through inhibiting nuclear factor-κB-mediated proinflammatory cytokine production.

Abstract: 

Moutan Cortex has been widely used to treat various types of arthritis in traditional Chinese medicine. Paeonol is isolated as an active ingredient from Moutan Cortex. However, the effect and potential mechanism of paeonol on gouty arthritis have not been evaluated. In this study, rats were treated intragastrically with paeonol for consecutive 7 days. On Day 5, rats were intra-articularly injected with monosodium urate (MSU) crystals in the ankle joints to induce MSU-induced arthritis (MIA). Paw volume was detected at various time points. Gait score was measured at 24 hr after MSU crystal injection. Ankle joints were collected for evaluation of histological score and expression of proinflammatory cytokines using hematoxylin and eosin staining and immunohistochemistry staining, respectively. Nuclear level of nuclear factor (NF)-κBp65 in synovial tissues was analyzed by western blot assay. NF-κB DNA-binding activity was measured by enzyme linked immunosorbent assay. Paeonol markedly lowered the paw volume, gait score, and histological score in MIA rats. Mechanistically, paeonol markedly reduced the expression of TNF-α, IL-1β, and IL-6 in synovial tissues of MIA rats. In addition, the elevated level of p65 in nucleus and NF-κB DNA-binding activity in synovial tissues of MIA rats were reduced significantly by paeonol treatment. These findings suggest that paeonol exerts anti-inflammatory effect in MIA rats throughinhibiting expression of proinflammatory cytokines and NF-κB activation.

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PMID: 

Neurochem Res. 2019 Nov ;44(11):2556-2565. Epub 2019 Sep 13. PMID: 31520267

Abstract Title: 

Anticonvulsant and Neuroprotective Effects of Paeonol in Epileptic Rats.

Abstract: 

Paeonol is the main active compound in the root bark extract of the peony tree, and it has antioxidative and anti-inflammatory effects. Recent studies have reported the neuroprotective effects of paeonol including its capacity in improving impaired memory. However, the effect of paeonol on epilepsy is yet to be demystified. We aimed to investigate the therapeutic effect of paeonol in epilepsy and its relationship with oxidative stress damage and neuronal loss in the rat brain to reveal the underlying mechanisms of epileptic seizures. A rat model for chronic epilepsy was established, and the seizure scores of the rats in different groups were recorded. The seizure duration and the seizure onset latency were used to evaluate the anticonvulsant effects of paeonol. Terminal deoxynucleotidyl transferase dUTP nick end-labeling staining, Nissl staining and H/E staining were used to evaluate the effects of paeonol on neuronal loss and apoptosis in epileptic rats. The colorimetric assessment of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, catalase activity and total antioxidant capacity of paeonol were used in assessing paeonol's effect on oxidative stress in epileptic rats. Evaluation of Caspase-3 mRNA and protein expression levels were determined using western blot and quantitative real-time (RT-q)PCR. In this study, we found that paeonol reduced the seizure scores of epileptic rats and attenuated the duration and onset latency of seizures. Paeonol can also increase the activities of total antioxidant capacity, SOD and catalase activity and reduce MDA content as well. This suggests that paeonol can improve the level of oxidative stress in rats. More significantly, paeonol can improve neuronal loss and apoptosis in epileptic rats. These results indicate that paeonol has anticonvulsant and neuroprotective effects in epileptic rats. This effect may be caused by reducing oxidative stress.

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PMID: 

J Photochem Photobiol B. 2019 Oct 16 ;200:111635. Epub 2019 Oct 16. PMID: 31671372

Abstract Title: 

Neuroprotective effect of biosynthesised gold nanoparticles synthesised from root extract of Paeonia moutan against Parkinson disease – In vitro&In vivo model.

Abstract: 

Parkinson disease is one of the most common neurological movement disorders affecting geriatric population. Biosynthesized gold nanoparticles are the ideal alternatives spotlighted by many researchers to treat various diseases. In the present study we synthesized gold nanoparticles using the root extract of Paeonia mountan, woody trees which are used in traditional Chinese medicine to be prescribed for diverse diseases. The synthesis of gold nanoparticles was confirmed with UV-Vis spectroscopic analysis and characterized using FTIR, HR-TEM, EDAX and XRD analysis. The cytotoxicity property of synthesized gold nanoparticles was assessed using MTT assay in the murine microglial BV2 cells. The neuroprotective effect of synthesized gold nanoparticles in inflammatory agent lipopolysaccharides triggered murine microglial BV2 cells was evaluated using nitric oxide, prostaglandin E2 and inflammatory cytokines assays such as IL-6&IL-1β. Further to confirm in vivo effect of synthesized nanoparticles, the nanoparticles were treated to Parkinson induced C57BL/6 mice. Behavioral, biochemical and molecular analysis were performed to estimate the potency of synthesized gold nanoparticles against the Parkinson induction in mice model.Our characterization results prove the gold nanoparticles synthesized using Paeonia mountan fulfills the requirement of ideal nanodrug and it potentially inhibited the inflammation in in vitro murine microglial BV2. The results of in vivo experiments authentically confirm gold nanoparticles synthesized using Paeonia mountan alleviates the neuroinflammation and improves the motor coordination in Parkinson induced mice.

PMID: 

Foods. 2019 Oct 10 ;8(10). Epub 2019 Oct 10. PMID: 31658783

Abstract Title: 

Phenolic Profile and Antioxidant Activity of the Edible Tree Peony Flower and Underlying Mechanisms of Preventive Effect on HO-Induced Oxidative Damage in Caco-2 Cells.

Abstract: 

The entire phenolic profiles and antioxidant activities of different organs of the edible tree peony flowers ((FDB)) were analyzed. HPLC-quadrupole time-of-flight mass spectrometer (Q-TOF-MS/MS) analyses of individual phenolic compounds revealed that the petal and stamen contained higher levels of flavonoid glycosides than other organs (

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PMID: 

Antioxidants (Basel). 2019 Oct 31 ;8(11). Epub 2019 Oct 31. PMID: 31683564

Abstract Title: 

White Peony (Fermented) Polyphenols Help Prevent Alcoholic Liver Injury via Antioxidation.

Abstract: 

White peony is a type of white tea () rich in polyphenols. In this study, polyphenols were extracted from white peony. In vitro experiments showed that white peony polyphenols (WPPs) possess strong free radical scavenging capabilities toward 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS). Long-term alcohol gavage was used to induce alcoholic liver injury in mice, and relevant indices of liver injury were examined. WPPs effectively reduced the liver indices of mice with liver injury. The serum levels of aspartate aminotransferase (ATS), alanine aminotransferase (ALT), alkaline phosphatase (ALP), triglycerides (TG), total cholesterol (TC), blood urea nitrogen (BUN), nitric oxide (NO), and malondialdehyde (MDA) were downregulated, while those of albumin (ALB), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were upregulated. WPPs also reduced the serum levels of interluekin-6 (IL-6), interluekin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ) in mice with liver injury. Pathology results showed that WPPs reduced alcohol-induced liver cell damage. Quantitative polymerase chain reaction (qPCR) and western blot results revealed that WPPs upregulated the mRNA and protein expressions of neuronal nitric oxidesynthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese superoxide dismutase (Mn-SOD), cupro-zinc superoxide dismutase (Cu/Zn-SOD), and CAT and downregulated iNOS expression in the liver of mice with liver injury. WPPs protected against alcoholic liver injury, and this effect was equivalent to that of silymarin. High-performance liquid chromatography revealed that WPPs mainly contained the polyphenols gallic acid, catechinic acid, and hyperoside, which are critical for exerting preventive effects against alcoholic liver injury. Thus, WPPs are high-quality natural products with liver protective effects.

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PMID: 

Cell Death Dis. 2019 Nov 7 ;10(11):846. Epub 2019 Nov 7. PMID: 31699976

Abstract Title: 

Cannabidiol promotes apoptosis via regulation of XIAP/Smac in gastric cancer.

Abstract: 

According to recent studies, Cannabidiol (CBD), one of the main components of Cannabis sativa, has anticancer effects in several cancers. However, the exact mechanism of CBD action is not currently understood. Here, CBD promoted cell death in gastric cancer. We suggest that CBD induced apoptosis by suppressing X-linked inhibitor apoptosis (XIAP), a member of the IAP protein family. CBD reduced XIAP protein levels while increasing ubiquitination of XIAP. The expression of Smac, a known inhibitor of XIAP, was found to be elevated during CBD treatment. Moreover, CBD treatment increased the interaction between XIAP and Smac by increasing Smac release from mitochondria to the cytosol. CBD has also been shown to affect mitochondrial dysfunction. Taken together, these results suggest that CBD may have potential as a new therapeutic target in gastric cancer.

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PMID: 

Eur J Orthop Surg Traumatol. 2019 Sep 20. Epub 2019 Sep 20. PMID: 31541301

Abstract Title: 

Influence of vitamin C on the incidence of CRPS-I after subacromial shoulder surgery.

Abstract: 

PURPOSE: The primary aim of this study was to determine whether postoperative administration of vitamin C (VC) is associated with reduced risk of complex regional pain syndrome type I (CRPS-I) after subacromial shoulder surgery (SaSS). The secondary objective of the study was to identify risk factor for the development of CRPS-I after SaSS.MATERIALS AND METHODS: A retrospective cohort study was performed to evaluate 542 patients undergoing SaSS from January 2015 to December 2016. The cohort was divided into two groups based on VC administration [Group I (no VC) and Group II (500 mg/day oral VC for 50 days postoperatively)]. The relationship between VC administration and development of CRPS-I was assessed. Demographics, preoperative clinical parameters, and operative variables were evaluated to determine their effect on the incidence of CRPS-I.RESULTS: A total of 267 patients (Group II) undergoing SaSS received VC, and 266 patients (Group I) did not. The incidence of CRPS-I was significantly different between two groups (36(13%) vs 18(7%), p = 0.009). Multivariable regression, however, demonstrated that VC reduced the risk of CRPS-I after SaSS by> 50% (aOR = 0.49; 95% CI 0.27-0.91). Patients undergoing open surgery (aOR = 2.19; 95% CI 1.2-4.0) were more likely to develop CRPS-I postoperatively. Higher preoperative Constant score (aOR = 0.94; 95% CI 0.91-0.98) was associated with lower risk for CRPS-I development.CONCLUSIONS: The present study found that VC administered prophylactically for 50 days postoperatively is effective in preventing CRPS-I development after SaSS. CRPS-I is a common complication following SaSS, especially in the setting of an open approach. The authors recommend preventive management with VC and arthroscopic approaches when possible for SaSS.LEVEL OF EVIDENCE III: Retrospective comparative study.

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