Crocin has pharmacological effects against the pathological behavior of colon cancer cells by interacting with the STAT3 signaling pathway.

PMID: 

Exp Ther Med. 2020 Feb ;19(2):1297-1303. Epub 2019 Dec 16. PMID: 32010302

Abstract Title: 

Crocin has pharmacological effects against the pathological behavior of colon cancer cells by interacting with the STAT3 signaling pathway.

Abstract: 

The aim of the present study was to investigate changes in proliferation, apoptosis, inflammation and chemokine release of colon cancer cells after treatment with crocin, as well as to investigate the signaling pathway that is regulated by crocin. The inhibition rates of different doses of crocin on the proliferation of HCT116 cells were measured by MTT assay. The ICwas calculated from the inhibition rates at 48 h. Proliferation curves of HCT116 cells were plotted after treatment with 271.18µM (high-dose group) or 135.6 µM (low-dose group) crocin. Flow cytometry and Hoechst 33342/propidium iodide double staining were used for detecting apoptosis. ELISA was used to measure the levels of macrophage inflammatory protein 2, interleukin (IL)-8, monocyte chemoattractant protein 1, tumor necrosis factor-α, IL-6 and IL-1β in the supernatant from cultured HCT116 cells following both high- and low-dose crocin treatment. Phosphorylated (P)-STAT3/STAT3 in HCT116 cells were measured by western blotting. Crocin inhibited the proliferation of HCT116 cells in a dose-dependent manner and thehigh-dose treatment with crocin resulted in a lower rate of proliferation. Additionally, crocin increased the apoptosis of HCT116 cells and the high-dose treatment with crocin led to a higher level of apoptosis. Notably, crocin decreased the secretion of chemokines and inflammatory factors from HCT116 cells and the high-dose treatment with crocin caused the greatest reduction in secretion of the factors. Crocin reduced the ratio of P-STAT3/STAT3, and thereby reduced the release of cytokines. The present study demonstrated that crocin may have pharmacological effects against the pathological behavior of colon cancer cells, and its mechanism of action may be related to the STAT3 signaling pathway.

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Essential oils of Rosa Damascena and Citrus Aurantium were both effective in improving the symptoms of premenstrual syndrome.

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PMID: 

J Family Med Prim Care. 2019 Sep ;8(9):2990-2996. Epub 2019 Sep 30. PMID: 31681680

Abstract Title: 

The effect of aromatherapy on mental, physical symptoms, and social functions of females with premenstrual syndrome: A randomized clinical trial.

Abstract: 

Objective: This study was designed to compare the effect of aromatherapy with Rosa Damascena and Citrus Aurantium blossom on psychological and physical symptoms and social functions of females with premenstrual syndrome.
Materials and Methods: This double-blind clinical trial was conducted on 95 students. They were randomly divided into three aromatherapy groups (aromatherapy with 4% concentration of Rosa Damascena and 0.5% concentration of Citrus Aurantium blossom essential oil) and aromatherapy with sweet almond oil (as control group). Premenstrual Symptoms Screening Tool questionnaire (PSST) was completed before and during the first and second month of the intervention. Data were analyzed by SPSS software version 22.
Results: After intervention, the scores of mental symptoms decreased in all three groups and this decrease was significant in both Citrus Aurantium (= 0.004) and Rosa Damascena groups (= 0.007). The score of physical symptoms was decreased in all three groups but it was significant only in the Rosa Demecensa group (= 0.042). The reduction of effect of symptoms on social function was observed in two intervention groups which were significant only in Rosa Damascena group (<0.001).
Conclusion: Essential oils of Rosa Damascena and Citrus Aurantium were both effective in improving the symptoms of premenstrual syndrome but the effect of Rosa Damascena, with regard to improvement of symptoms of premenstrual syndrome was more than that of Citrus Aurantium in all psychological, physical, and social aspects.

Rose hydrosol exerts significant protective properties in diabetes mellitus.

PMID: 

Molecules. 2019 Nov 10 ;24(22). Epub 2019 Nov 10. PMID: 31717650

Abstract Title: 

Effects of Orally ConsumedMill. Hydrosol on Hematology, Clinical Chemistry, Lens Enzymatic Activity, and Lens Pathology in Streptozotocin-Induced Diabetic Rats.

Abstract: 

Diabetes mellitus is a multisystemic metabolic disorder that may affect the eyes, kidneys, vessels, and heart. Chronic hyperglycemia causes non-enzymatic glycation of proteins and elevation of the polyol pathway resulting in oxidative stress that damages organs. The current study aimed to investigate the dose-dependent effects of orally consumedMill. hydrosol on hematology, clinical biochemistry, lens enzymatic activity, and lens pathology in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced into male Sprague-Dawley rats by intraperitoneal administration of STZ (40 mg/kg body weight). Rose hydrosols containing 1515 mg/L and 500 mg/L total volatiles (expressed as citronellol) were introduced to rats orally for 45 days. Consumption of 1515 mg/L volatile containing rose hydrosol successfully ameliorated hematologic, hepatic, and renal functions. Hydrosols also attenuated hyperglycemia and decreased the advanced glycation end-product formation in a dose-dependent manner. Rose hydrosol components significantly increased the lens enzymatic activities of glutathione peroxidase and decreased the activity of aldose reductase to prevent cataractogenesis. Histopathological examinations of rat lenses also indicated that increasing the dose of rose hydrosol had a protective effect on lenses in diabetic conditions. Additionally, in silico modeling of aldose reductase inhibition with rose hydrosol volatiles was carried out for extrapolating the current study to humans. The present results suggest that rose hydrosol exerts significant protective properties in diabetes mellitus and has no toxic effect on all studied systems in healthy test groups.

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The herbal extract ALS-L1023 from Melissa officinalis alleviates visceral obesity and insulin resistance in obesity.

PMID: 

J Ethnopharmacol. 2020 Feb 3:112646. Epub 2020 Feb 3. PMID: 32027997

Abstract Title: 

The herbal extract ALS-L1023 from Melissa officinalis alleviates visceral obesity and insulin resistance in obese female C57BL/6J mice.

Abstract: 

ETHNOPHARMACOLOGICAL RELEVANCE: Melissa officinalis L. (Labiatae; lemon balm) has traditionally been used as a medicinal herb to treat stress, anxiety, and insomnia. Current reports suggest that not only chronic stress stimulates angiogenesis, but angiogenesis also regulates adipogenesis and obesity. Because the herbal extract ALS-L1023 from Melissa officinalis inhibits angiogenesis, we hypothesized that ALS-L1023 could suppress visceral obesity and insulin resistance in obese female C57BL/6J mice, a mouse model of obese premenopausal women.MATERIALS AND METHODS: The mice were grouped and fed for 16 weeks as follows: 1) low-fat diet (LFD), 2) high-fat diet (HFD), or 3) HFD supplemented with 0.4 or 0.8% ALS-L1023. Variables and determinants of visceral obesity, insulin resistance, and pancreatic dysfunction were then assessed via blood analysis, histology, immunohistochemistry, and real-time polymerase chain reaction.RESULTS: ALS-L1023 decreased weight gain, visceral adipocyte size, and serum lipid levels in HFD-fed obese mice. ALS-L1023 also normalized hyperglycemia and hyperinsulinemia and concomitantly reduced blood glucose levels during oral glucose tolerance tests. The pancreatic islet size and insulin-positiveβ-cell area were significantly reduced in ALS-L1023-treated mice compared with untreated obese controls, reaching a level similar to that of LFD-fed lean mice. ALS-L1023 suppressed pancreatic lipid accumulation, infiltration of inflammatory cells, and collagen levels. ALS-L1023 treatment altered the pancreatic expression of genes involved in steatosis, inflammation, and fibrosis.CONCLUSIONS: Our findings indicate that the herbal extract ALS-L1023 from Melissa officinalis not only inhibits visceral obesity, but also attenuates the increased fasting blood glucose, impaired glucose tolerance, and pancreatic dysfunction seen in female obese mice. These results suggest that ALS-L1023 may be effective in the prevention of visceral obesity and insulin resistance in obese premenopausal women.

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An essential oil-loaded hydrogel had the potential to provide a novel antimicrobial therapy for the treatment of oral candidiasis.

PMID: 

Microorganisms. 2020 Feb 6 ;8(2). Epub 2020 Feb 6. PMID: 32041100

Abstract Title: 

Methylcellulose Hydrogel withEssential Oil as a Potential Treatment for Oral Candidiasis.

Abstract: 

spp. are the most prevalent fungi of the human microbiota and are opportunistic pathogens that can cause oral candidiasis. Management of such infections is limited due to the low number of antifungal drugs available, their relatively high toxicity and the emergence of antifungal resistance. Therefore, much interest in the antimicrobial potential of natural compounds has recently been evident. The use of hydrogels in the delivery of biocides has been explored due to their biocompatibility, ease with drug encapsulation, and due to their potential to confer mechanical and structural properties similar to biological tissue. Methylcellulose hydrogels (10% (/)) with 1% (/) and 2% (/)oil were synthesised. The rheological properties and gelation time of the hydrogels were evaluated. Antimicrobial action, the antifungal potential and ability to displacewere determined. Rheological tests revealed that the hydrogel jellified in three minutes at 37°C. Loaded hydrogels successfully inhibitedgrowth as evident by zone of inhibition and time-kill assays. A significant reduction in retainedwas demonstrated with the hydrogel at 2%concentration. This work demonstrated that an essential oil-loaded hydrogel had the potential to provide a novel antimicrobial therapy for the treatment of oral candidiasis.

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Isoliquiritigenin inhibits mouse S180 tumors with a new mechanism that regulates autophagy by GSK-3β/TNF-α pathway.

PMID: 

Eur J Pharmacol. 2018 Nov 5 ;838:11-22. Epub 2018 Aug 29. PMID: 30171855

Abstract Title: 

Isoliquiritigenin inhibits mouse S180 tumors with a new mechanism that regulates autophagy by GSK-3β/TNF-α pathway.

Abstract: 

In this study, the pharmacokinetic properties and stability of isoliquiritigenin (ILQ) in microsomes were evaluated. The data showed ILQ administrated by i.h had high absorption degree (absolute bioavailability>90%), and strong elimination ability (average t≈ 67 min). ILQ in rat tissues could reach peak at 0.25 h, and be detected in almost all tissues. In vitro, stability of ILQ in four species liver microsomes were rat> beagle dog> monkey> human> mouse. On the basis of pharmacokinetic (PK) profiles, mechanism of ILQ against S180 was explored. ILQ could not inhibit S180 growth directly in vitro. However, ILQ extremely prohibited S180 tumor volume in vivo. And when TNF-α in NK cells was knocked down by siRNA, ILQ had no inhibiting effect on S180 tumor. ILQ enhanced TNF-α expression in NK cells by FCM detection. Autophagy-associated proteins LC3-II, Beclin-1, ATG-7 were elevated in S180 cells co-cultured with ILQ treating NK cells. When TNF-α was knocked down by siRNA, ILQ could not induce autophagy in S180 tumors. In the NK cells of osteosarcoma patients, TNF-α was negatively correlated with GSK-3β by ELISA detection. ILQ could inhibit GSK-3β expression and further increased p65 and c-Rel expression in NK cells. When GSK-3β was knocked down by siRNA, ILQ did not affect p65 and c-Rel expression. ILQ directly inhibited GSK-3β and then activated the NF-κB pathway to enhance TNF-α expression in NK cells, which could induce autophagy in sarcomas. The present study supplied a new mechanism for ILQ against tumors.

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Neuroprotective effects of liquiritin on cognitive deficits induced by soluble amyloid-β1-42 oligomers injected into the hippocampus.

PMID: 

J Asian Nat Prod Res. 2016 Dec ;18(12):1186-1199. Epub 2016 Sep 2. PMID: 27589374

Abstract Title: 

Neuroprotective effects of liquiritin on cognitive deficits induced by soluble amyloid-βoligomers injected into the hippocampus.

Abstract: 

This study assessed the modulating effects of liquiritin against cognitive deficits, oxidative damage, and neuronal apoptosis induced by subsequent bilateral intrahippocampal injections of aggregated amyloid-β(Aβ). This study also explored the molecular mechanisms underlying the above phenomena. Liquiritin was orally administered to rats with Aβ-induced cognitive deficits for 2 weeks. The protective effects of liquiritin on the learning and memory impairment induced by Aβwere examined in vivo by using Morris water maze. The rats were then euthanized for further studies. The antioxidant activities of liquiritin in the hippocampus of the rats were investigated by biochemical and immunohistochemical methods. The apoptosis of the neurons was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling assay. Liquiritin at doses of 50-100 mg/kg significantly improved the cognitive ability, restored the abnormal activities of glutathione peroxidase and superoxide dismutase, and decreased the levels of malondialdehyde,8-hydroxy-2'-deoxyguanosine and protein carbonyl in the hippocampus of rats with Alzheimer's disease. Moreover, neural apoptosis in the hippocampus of Aβ-treated rats was reversed by liquiritin. Liquiritin can significantly ameliorate Aβ-induced spatial learning and memory impairment by inhibiting oxidative stress and neural apoptosis.

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The protective role of liquiritin in high fructose-induced myocardial fibrosis.

PMID: 

Biomed Pharmacother. 2016 Dec ;84:1337-1349. Epub 2016 Nov 1. PMID: 27810791

Abstract Title: 

The protective role of liquiritin in high fructose-induced myocardial fibrosis via inhibiting NF-κB and MAPK signaling pathway.

Abstract: 

Diabetic cardiomyopathy has been known as an important complication of diabetes and characterized by persistent diastolic dysfunction, resulting in myocardial fibrosis, which is associated inflammatory response and oxidative stress. Liquiritin is a major constituent of Glycyrrhiza Radix, possessing various pharmacological activities and exhibiting various positive biological effects, including anti-cancer, anti-oxidative and neuroprotective effects. Here, we investigated the anti-inflammatory properties and protective effects of lquiritin in high fructose-induced mice and cardiomyocytes to clarify the potential mechanism. The mice were divided into the control mice, 30% high fructose-induced mice, 10mg/kg liquiritin-treaed mice after fructose feeding and 20mg/kg liquiritin-treaed mice after fructose feeding. Liquiritin effectively reduced the lipid accumulation and insulin resistance induced by fructose feeding. In comparison to high fructose-feeding control mice, liquiritin-treated mice developed less myocardial fibrosis with lower expression of Collagen type I, Collagen type II and alpha smooth muscle-actin (α-SMA). In addition, liquiritin significantly reduced the inflammatory cytokine release and NF-κB phosphorylation through IKKα/IκBα signaling pathway suppression. Further, Mitogen-activated protein kinases (MAPKs), including p38, ERK1/2 and JNK, was up-regulated for fructose stimulation, whichwas inactivated by liquiritin treatment in vivo and in vitro studies. Our data indicates that liquiritin has a protective effect against high fructose-induced myocardial fibrosis via suppression of NF-κB and MAPKs signaling pathways, and liquiritin may be a promising candidate for diabetes-relatedmyocardial fibrosis treatment.

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Sleep-inducing effect of Passiflora incarnata L. extract by single and repeated oral administration.

PMID: 

Food Sci Nutr. 2020 Jan ;8(1):557-566. Epub 2019 Dec 19. PMID: 31993179

Abstract Title: 

Sleep-inducing effect ofextract by single and repeated oral administration in rodent animals.

Abstract: 

Social cost of insomnia in modern society is gradually increasing. Due to various social phenomena and lifestyles that take away the opportunity of good quality of sleep, problems of insomnia cannot be easily figured out. Prescription of sleeping pills for insomnia patients can cause other inconveniences due to their side effects beyond their intended purposes. On the other hand,(PI) has been widely used in South America for several centuries, showing effectiveness for sleep, sedation, anxiety, and so on in the civilian population. However, reports on the treatment efficacy of this herbal medicinal plant for insomnia patients through standardization as a sleeping agent have been very rare. Therefore, we obtained leaves and fruits of PI (8:2 by weight) as powder to prepare an extract. It was then applied to C6 rat glioma cells to quantitate mRNA expression levels of GABA receptors. Its sleep-inducing effect was investigated using experimental animals. PI extract (6 μg/ml) significantly decreased GABA receptors at 6 hr after treatment. Immobility time and palpebral closing time were significantly increased after single (500 mg/kg) or repeated (250 mg/kg) oral administration. In addition, blood melatonin levels were significantly increased in PI extract-treated animals after both single and repeated administrations. These results were confirmed through several repeated experiments. Taken together, these results confirmed that PI extract had significant sleep-inducing effects in cells and animals, suggesting that PI extract might have potential for treating human insomnia.

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