Analgesic, anti-inflammatory, and central nervous system depressant activities of Monochoria hastate (L.) Solms. in animal models

2020 ◽  
Vol 16 (71) ◽  
pp. 580
Author(s):  
Tufael Ahmed ◽  
LuthfunMst Nesa ◽  
DA Anwar Al-Aman ◽  
IslamNazrul Kazi ◽  
MdEleas Kobir ◽  
...  
2020 ◽  
Vol 11 (3) ◽  
pp. 9836-9847

Lavandulae aetheroleum, the oil, was obtained by vapor condensation from the flower of Lavandula angustifolia Mill. or Lavandula intermedia Loisel (Lamiaceae) plant. Other names of Lavandulae aetheroleum oil are Al birri, common or English lavender. The Lavandula angustifolia Mill. or Lavandula intermedia Loisel plant is spreading in the Mediterranean, southern Europe, Bulgaria, Russia, and USA. The Lavandula angustifolia Mill. or Lavandula intermedia Loisel plant, is an odor shrub with 1-2 m in height. The oil is a clear, colorless, or pale yellow. The gas chromatography studies reported the following percentage of the major chemical constituents in the oil: linalyl acetate (25-46%), linalool (20-45%), terpinen-4-ol (1.2-6.0%), lavendulyl acetate (> 1.0%), 1,8-cineole (1,8-cineol, cineol, cineole, eucalyptol) (< 2.5%), 3-octanone (< 2.5%), camphor (< 1.2%), limonene (< 1.0%), and α-terpineol (< 2.0%). Medicinal applications of the oil include the treatment of restlessness, anxiety, cardiovascular disorders, insomnia, and gastrointestinal disorders, burns, diarrhea, headache, sore throats, and wounds. Pharmacological effects include experimental and clinical pharmacology. Experimental pharmacology includes anesthetic, anticonvulsant, sedative, anti-inflammatory, antimicrobial, antispasmodic, antispasmodic, central nervous system depressant effects. Clinical pharmacology includes anxiolytic, analgesic, and cardiovascular effects. The oil dose by inhalation = 0.06-0.2 ml/ 3 times/day while oil dose internally = 1-4 drops approximately 20-80 mg on a sugar cube per day. In conclusion, Lavandulae aetheroleum oil had an anesthetic, anticonvulsant, sedative, anti-inflammatory, antimicrobial, antispasmodic, antispasmodic, central nervous system depressant, anxiolytic, analgesic, and cardiovascular effects.


2018 ◽  
Vol 8 (5-s) ◽  
pp. 41-46
Author(s):  
Bhagat Singh Jaiswal ◽  
Mukul Tailang

Argyreia speciosa (Linn.f.) (Family: Convolvulaceae, Synonyms: Argyreia nervosa) is used in the traditional Ayurvedic systems of medicine as well as in local health folklore. It is commonly known as Vidhaara in Hindi and Hawaiian Baby Woodrose and Elephant creeper in English. It is the large climber and seen throughout India up to an altitude of 500 m. A. speciosa possess various pharmacological activity such as anti-aging, gastroprotective, analgesic & anti-inflammatory, aphrodisiac, antiviral, antidiabetic,  anticonvulsion, antioxidant, antidiarrheal, antiulcer, central nervous system depressant, nematocides, nootropic, anticancer and many more. Apart from this numerous phytoconstituents have been isolated from A. speciosa. Its seeds principally contain lysergamides, eragine and isoeragine which responsible for its hallucinogenic properties. The present paper efforts bring to light the available literature on A. speciosa with respect to traditional, ethnobotanical, phytoconstituents and review of different pharmacological activities. Keywords: Argyreia speciosa, Vidhaara, Anti-aging, Hallucinogen, Ethnobotanical


2020 ◽  
Author(s):  
Carolina Prado ◽  
Francisco Osorio-Barrios ◽  
Alexandra Espinoza ◽  
Juan J Saez ◽  
María I Yuseff ◽  
...  

Abstract Background: Recent evidence has shown dopamine as a major regulator of inflammation. Accordingly, dopaminergic regulation of adaptive and innate immune cells plays an important role in the physiopathology of inflammatory disorders. Multiple sclerosis (MS) is an inflammatory disease involving a CD4+ T-cell-driven autoimmune response to central nervous system (CNS) derived antigens. Evidence from animal models has suggested that B-cells play a fundamental role as antigen-presenting cells (APC) re-stimulating CD4+ T-cells in the CNS as well as regulating T-cell response by mean of inflammatory or anti-inflammatory cytokines. Here we addressed the role of the dopamine receptor D3 (DRD3), which display the highest affinity for dopamine, in B-cells in animal models of MS.Methods: Mice harbouring Drd3-deficient or Drd3-suficient B-cells were generated by bone marrow transplantation into recipient mice devoid of B-cells. In these mice we compare the development of experimental autoimmune encephalomyelitis (EAE) induced by immunization with a myelin oligodendrocyte glycoprotein (MOG)-derived peptide (pMOG), a model that leads to CNS-autoimmunity irrespective of the APC function of B-cells, or by immunization with full-length human MOG protein (huMOG), a model in which antigen-specific activated B-cells display a fundamental APCs function in the CNS. Results: Our data shows that, by promoting the expression of the chemokine receptor CXCR3 in autoreactive B-cells, DRD3-stimulation favours the CNS-tropism in a subset of B-cells that act as APC in the CNS, which is fundamental for disease development. Furthermore, we found that DRD3- stimulation induced the expression of the CNS-homing molecule CD49d in a B-cell subset with anti-inflammatory features, thus attenuating EAE manifestation in a CNS-autoimmunity model independent of the APC function of B-cells.Conclusion: Our findings demonstrate that DRD3-stimulation in B-cells exerts a dual role in CNS-autoimmunity, favouring CNS-tropism of pro-inflammatory B-cells with APC function, and also promoting CNS-homing of B-cells with anti-inflammatory features. Thus, these results show DRD3-stimulation in B-cells as a key regulator of CNS-autoimmunity.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Carolina Prado ◽  
Francisco Osorio-Barrios ◽  
Paulina Falcón ◽  
Alexandra Espinoza ◽  
Juan José Saez ◽  
...  

Abstract Background Recent evidence has shown dopamine as a major regulator of inflammation. Accordingly, dopaminergic regulation of immune cells plays an important role in the physiopathology of inflammatory disorders. Multiple sclerosis (MS) is an inflammatory disease involving a CD4+ T-cell-driven autoimmune response to central nervous system (CNS) derived antigens. Evidence from animal models has suggested that B cells play a fundamental role as antigen-presenting cells (APC) re-stimulating CD4+ T cells in the CNS as well as regulating T-cell response by mean of inflammatory or anti-inflammatory cytokines. Here, we addressed the role of the dopamine receptor D3 (DRD3), which displays the highest affinity for dopamine, in B cells in animal models of MS. Methods Mice harbouring Drd3-deficient or Drd3-sufficient B cells were generated by bone marrow transplantation into recipient mice devoid of B cells. In these mice, we compared the development of experimental autoimmune encephalomyelitis (EAE) induced by immunization with a myelin oligodendrocyte glycoprotein (MOG)-derived peptide (pMOG), a model that leads to CNS-autoimmunity irrespective of the APC-function of B cells, or by immunization with full-length human MOG protein (huMOG), a model in which antigen-specific activated B cells display a fundamental APC-function in the CNS. APC-function was assessed in vitro by pulsing B cells with huMOG-coated beads and then co-culturing with MOG-specific T cells. Results Our data show that the selective Drd3 deficiency in B cells abolishes the disease development in the huMOG-induced EAE model. Mechanistic analysis indicates that although DRD3-signalling did not affect the APC-function of B cells, DRD3 favours the CNS-tropism in a subset of pro-inflammatory B cells in the huMOG-induced EAE model, an effect that was associated with higher CXCR3 expression. Conversely, the results show that the selective Drd3 deficiency in B cells exacerbates the disease severity in the pMOG-induced EAE model. Further analysis shows that DRD3-stimulation increased the expression of the CNS-homing molecule CD49d in a B-cell subset with anti-inflammatory features, thus attenuating EAE manifestation in the pMOG-induced EAE model. Conclusions Our findings demonstrate that DRD3 in B cells exerts a dual role in CNS-autoimmunity, favouring CNS-tropism of pro-inflammatory B cells with APC-function and promoting CNS-homing of B cells with anti-inflammatory features. Thus, these results show DRD3-signalling in B cells as a critical regulator of CNS-autoimmunity.


2021 ◽  
Vol 11 (5) ◽  
pp. 12886-12900

The dried aerial parts of Passiflora incarnate L. plant are called Herba Passiflorae. This plant belongs to the Passifloraceae family. This review aims to focus on the importance of Herba Passiflorae in medicinal applications with special reference to its experimental and clinical pharmacology. Herba Passiflorae possesses flavonoids and alkaloids ingredients. The major constituents of Herba Passiflorae are flavonoids such as vicenin-2, orientin, isoorientin, vitexin, and isovitexin. Herba Passiflorae is applied for the cure of dysmenorrhoea, neuralgia, and nervous tachycardia. It is a slight sedative for nervous restlessness, insomnia, and anxiety. The fruit of Herba Passiflorae is used for jams, jellies, and desserts. The juice is a favorite flavoring in drinks. The pharmacology effect of Herba Passiflorae includes experimental and clinical pharmacology. Experimental pharmacology includes analgesic, antipyretic, anti-inflammatory, antimicrobial, cardiovascular, central nervous system depressant, and uterine stimulant effects. Clinical pharmacology includes anxiolytic, analgesic, and sedative effects, as well as its effect on nausea, menopause, dysmenorrhea, and diabetes. Herba Passiflorae stimulates uterine contractions, so it is used during pregnancy. The water extract of Herba Passiflorae is not genotoxic. The passion fruit is more appropriate for children's use due to the incorporation of Lactobacillus casei in passion fruit. The daily oral intake of passion fruit at public doses is non-toxic and safe. The daily dose in adults as a sedative is 0.5-2 g of aerial parts 3-4 times. In conclusion, Herba Passiflorae has analgesic, antipyretic, anti-inflammatory, antimicrobial, cardiovascular, central nervous system depressant, uterine stimulant, anxiolytic, analgesic, and sedative effects, as well as, its effect on nausea, menopause, dysmenorrhea, and diabetes.


2021 ◽  
Author(s):  
Carolina Prado ◽  
Francisco Osorio-Barrios ◽  
Alexandra Espinoza ◽  
Juan J Saez ◽  
María I Yuseff ◽  
...  

Abstract Background. Recent evidence has shown dopamine as a major regulator of inflammation. Accordingly, dopaminergic regulation of adaptive and innate immune cells plays an important role in the physiopathology of inflammatory disorders. Multiple sclerosis (MS) is an inflammatory disease involving a CD4+ T-cell-driven autoimmune response to central nervous system (CNS) derived antigens. Evidence from animal models has suggested that B-cells play a fundamental role as antigen-presenting cells (APC) re-stimulating CD4+ T-cells in the CNS as well as regulating T-cell response by mean of inflammatory or anti-inflammatory cytokines. Here we addressed the role of the dopamine receptor D3 (DRD3), which display the highest affinity for dopamine, in B-cells in animal models of MS. Methods. Mice harbouring Drd3-deficient or Drd3-suficient B-cells were generated by bone marrow transplantation into recipient mice devoid of B-cells. In these mice we compare the development of experimental autoimmune encephalomyelitis (EAE) induced by immunization with a myelin oligodendrocyte glycoprotein (MOG)-derived peptide (pMOG), a model that leads to CNS-autoimmunity irrespective of the APC function of B-cells, or by immunization with full-length human MOG protein (huMOG), a model in which antigen-specific activated B-cells display a fundamental APCs function in the CNS.Results. Our data shows that, by promoting the expression of the chemokine receptor CXCR3 in autoreactive B-cells, DRD3-stimulation favours the CNS-tropism in a subset of B-cells that act as APC in the CNS, which is fundamental for disease development. Furthermore, we found that DRD3- stimulation induced the expression of the CNS-homing molecule CD49d in a B-cell subset with anti-inflammatory features, thus attenuating EAE manifestation in a CNS-autoimmunity model independent of the APC function of B-cells.Conclusions. Our findings demonstrate that DRD3-stimulation in B-cells exerts a dual role in CNS-autoimmunity, favouring CNS-tropism of pro-inflammatory B-cells with APC function, and also promoting CNS-homing of B-cells with anti-inflammatory features. Thus, these results show DRD3-signalling in B-cells as a key regulator of CNS-autoimmunity.


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