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The Pharmacological Properties of Silymarin and Its Constituents
Lucia Dwi Antika,Rita Marleta Dewi 한국생약학회 2021 Natural Product Sciences Vol.27 No.2
Silymarin is a standardized extract obtained from the seeds and fruits of Silybum marianum L., or commonly called milk thistle, a member of Carduus marianum family that contains mix of flavonolignans. Some epidemiological and preclinical studies revealed that S. marianum L. has been used for herbal remedies for centuries for its pharmacological activity. In this review, pharmacological studies in vitro and in vivo of silymarin are discussed thoroughly stressing on antioxidant, antimicrobial, antiviral, and anti-carcinogenic aspects of silymarin. In addition, the protective influences of silymarin on some organs such as heart, liver, bone, and neuron tissue are reviewed as well. This review would be useful for further study regarding the potential of natural plant, notably silymarin, and its therapeutic potential in the prevention and treatment of diseases.
Parvidepsidone, a Novel Depsidone from the Barks of Garcinia parvifolia Miq.
Sri Hartati,Megawati Megawati,Lucia Dwi Antika 한국생약학회 2022 Natural Product Sciences Vol.28 No.1
Garcinia parvifolia Miq., belongs to Garcinia genus and Clusiaceae family, is one of the well-known species from Garcinia genus which widely found in tropical and subtropical countries, and has been reported to contain natural bioactive compounds. A novel depsidone, parvidepsidone (2), was isolated from the barks of G. parvifolia along with two known compounds: stigmasterol (1) and rubraxhantone (3). Based on information of LC-MS, 1D and 2D NMR spectra, the structure of parvidepsidone (2) was fully assigned.
Shin, Daekeun,Park, Sin-Hye,Choi, Yean-Jung,Kim, Yun-Ho,Antika, Lucia Dwi,Habibah, Nurina Umy,Kang, Min-Kyung,Kang, Young-Hee MDPI 2015 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.16 No.12
<P>Asthma is characterized by aberrant airways including epithelial thickening, goblet cell hyperplasia, and smooth muscle hypertrophy within the airway wall. The current study examined whether kaempferol inhibited mast cell degranulation and prostaglandin (PG) release leading to the development of aberrant airways, using an <I>in vitro</I> model of dinitrophenylated bovine serum albumin (DNP-BSA)-sensitized rat basophilic leukemia (RBL-2H3) mast cells and an <I>in vivo</I> model of BSA-challenged asthmatic mice. Nontoxic kaempferol at 10–20 μM suppressed β-hexosaminidase release and cyclooxygenase 2 (COX2)-mediated production of prostaglandin D2 (PGD2) and prostaglandin F2α (PGF2α) in sensitized mast cells. Oral administration of ≤20 mg/kg kaempferol blocked bovine serum albumin (BSA) inhalation-induced epithelial cell excrescence and smooth muscle hypertrophy by attenuating the induction of COX2 and the formation of PGD2 and PGF2α, together with reducing the anti-α-smooth muscle actin (α-SMA) expression in mouse airways. Kaempferol deterred the antigen-induced mast cell activation of cytosolic phospholipase A2 (cPLA2) responsive to protein kinase Cμ (PKCμ) and extracellular signal-regulated kinase (ERK). Furthermore, the antigen-challenged activation of Syk-phospholipase Cγ (PLCγ) pathway was dampened in kaempferol-supplemented mast cells. These results demonstrated that kaempferol inhibited airway wall thickening through disturbing Syk-PLCγ signaling and PKCμ-ERK-cPLA2-COX2 signaling in antigen-exposed mast cells. Thus, kaempferol may be a potent anti-allergic compound targeting allergic asthma typical of airway hyperplasia and hypertrophy.</P>
Astragalin Inhibits Allergic Inflammation and Airway Thickening in Ovalbumin-Challenged Mice
Kim, Yun-Ho,Choi, Yean-Jung,Kang, Min-Kyung,Park, Sin-Hye,Antika, Lucia Dwi,Lee, Eun-Jung,Kim, Dong Yeon,Kang, Young-Hee American Chemical Society 2017 Journal of agricultural and food chemistry Vol.65 No.4
<P>Lung inflammation and oxidative stress are the major contributors to the development of obstructive pulmonary diseases. Macrophages are involved in pulmonary inflammation and alveolar damage in emphysema. Astragalin is an anti-inflammatory flavonoid present in persimmon leaves and green tea seeds. This study elucidated that astragalin inhibited inflammatory cell infiltration induced by 20 mu M H2O2 and blocked airway thickening and alveolar emphysema induced by 20 pig of ovalbumin (OVA) in mice. OVA induced mouse pulmonary MCP-1, and H2O2 enhanced the expression of MCP-1/ICAM-1/ccv integrin in bronchial airway epithelial BEAS-2B cells. Such induction was inhibited by supplying 10-20 mg/kg of astragalin to OVA-challenged mice and 1-20 mu M astragalin to oxidant-stimulated cells. Oral administration of 20 mg/kg of astragalin reduced the induction of F4/80/CD68/CD11b in airways of mice challenged with OVA. Additionally, emphysema tissue damage was observed in OVA-exposed alveoli. Mast cell recruitment in the airway subepithelium was blocked by supplementing astragalin to OVA-challenged mice. Orally treating 20 mg/kg of astragalin reduced alpha-SMA. induction in inflammation-occurring airways and appeared to reverse airway thickening and constriction induced by an OVA episode. These results revealed that astragalin may improve airway thickening and alveolar destruction with blockade of allergic inflammation in airways. Therefore, astragalin may be a therapeutic agent antagonizing asthma and obstructive pulmonary diseases.</P>