Platycodin D and D3 Increase Airway Mucin Release in vivo and in vitro in Rats and Hamsters

Shin, Chan Young; Lee, Woo Jong; Lee, Eun Bang; Choi, Eui Yul; Ko, Kwang Ho

doi:10.1055/s-2002-23130

Cited by 76 publications

(46 citation statements)

References 17 publications

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“…1 Although many compounds have been isolated from P. grandiflorum roots, PD has shown the most potent biological activities of all the platycodin saponins. [2][3][4][5][6][7] Recent studies have shown that PD effectively induces apoptosis in many cancer cells; 8,9 however, the underlying cellular and molecular mechanisms responsible for PD's anticancer activity in human leukemia cells are not known. In our study, we first provided the apoptotic mechanisms induced by PD in leukemia cells.…”

Section: Discussionmentioning

confidence: 99%

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Platycodin D induces mitotic arrest in vitro, leading to endoreduplication, inhibition of proliferation and apoptosis in leukemia cells

Kim

Moon

Choi

et al. 2008

Intl Journal of Cancer

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Platycodin D (PD), a major constituent of triterpene saponins in Platycodon grandiflorum, has also become an interesting candidate for cancer chemotherapy; however, little is known about apoptotic mechanisms on cancer cells. We herein investigated the mechanisms that are related to PD-induced antiproliferation and cell death in human leukemia cells (U937, THP-1 and K562 cells). Cell growth was assessed with proliferation assays, cell counting, flow cytometry, phase contrast microscopy and Western blot assay. Microtubule (MT) formation was measured with immunofluorescent staining and in vitro tubulin polymerization assay. Apoptotic effect was analyzed by assessing increase in annexin V-staining and caspase-3 activity. Treatment of synchronized leukemia cells with varying concentrations of PD resulted in significant mitotic arrest and endoreduplication (END) via downregulation of Cdc2/ cyclin B1 and upregulation of wee1 expression, and elevated the Cdk2 protein via downregulation of p21 within 48 hr. We also researched PD's induction of polyploidy through the MT polymerization. Immunofluorescent microscopy and Western blot analysis revealed that PD significantly caused MT polymerization in leukemia cells. We also found that very high concentrations of PD (>200 lM) were required to directly induce MT polymerization in vitro. Finally, PD exposure induced apoptosis in U937 cells through caspase-3-dependent PARP and lamin A cleavage. We conclude that the primary antileukemia activity of PD is induction of endoreduplication and mitotic arrest, as a consequence of suppressing spindle MT dynamics and in promoting apoptosis in human leukemia cells.

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Section: Discussionmentioning

confidence: 99%

“…PD contains a crucial bioactive component responsible for diverse effects such as anti-inflammatory, antiallergic and cholesterol-lowering activities. [3][4][5][6][7] Although recent studies have also shown that PD can induce apoptosis in several cancer cells, 8,9 until now no clear or unique mechanisms of PD-induced apoptosis are known.…”

mentioning

confidence: 99%

Platycodin D induces mitotic arrest in vitro, leading to endoreduplication, inhibition of proliferation and apoptosis in leukemia cells

Kim

Moon

Choi

et al. 2008

Intl Journal of Cancer

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“…19) Saponins (PS) are the primary constituents of Platycodi Radix, [20][21][22] and they are responsible for diverse effects including anti-inflammation, [23][24][25][26] anti-allergy, 23) anti-tumor, 27) augmentation of immune response, [28][29][30] and stimulating the apoptosis in skin cells. 27) In the last decade, PS has generated renewed interests due to their pharmacological potentials for healing the diseases of adulthood such as hyperlipidemia or anti-obesity.…”

Section: )mentioning

confidence: 99%

Anti-inflammatory Activity of Prosapogenin Methyl Ester of Platycodin D via Nuclear Factor-kappaB Pathway Inhibition

Chung

Noh

Zhao

et al. 2008

Biological & Pharmaceutical Bulletin

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Immune responses to infection or to localized injury or trauma are among the main causes of local or systemic inflammation. Despite the beneficial effect of inflammation in limiting responses to cellular and organ damage, a breakdown in the regulation of the inflammatory response may result in a wide range of chronic diseases such as arthritis, inflammatory bowel diseases, asthma and others. 1)Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, sulindac and indomethacin, are widely believed to have anti-inflammatory effects due to their ability to inhibit prostanoid production, and relieve inflammation by inhibiting cyclooxygenase (COX).COX are the rate-limiting enzymes that catalyze the formation of prostaglandins from arachidonic acid.2-5) Levels of prostaglandins increase early in the course of the inflammatory process. The constitutive isoform, COX-1, is expressed in most tissues predominantly in platelets, gastrointestinal tract, kidney, and liver.2-4) The inducible isoform, COX-2, is activated in response to pro-inflammatory cytokines and growth factors.3,4) Because COX-2 protein is induced by several kinds of stimuli in inflammatory cells, inhibitors of COX-2 protein induction might be candidates for the new-type NSAIDs. Also, inflammation is associated with inducible nitric oxide synthase (iNOS). Especially, nitric oxide (NO) produced by activated macrophages via iNOS was initially considered a component of innate immunity in the fight against infections. 6) It has been well accepted that nuclear-factor-kB (NF-kB) signaling pathway plays important roles in the inflammation, control of cell growth, apoptosis, stress response, and many other physiological processes. [7][8][9][10][11] There are several important molecules such as NF-kB, inhibitor kB (IkB), IKK, within NF-kB signaling pathway.12) NF-kB is a key protein in the pathway, and has been described as a major culprit and a therapeutic target in inflammation and cancer. [13][14][15][16] It is activated by lipopolysaccharide (LPS), which is a mammalian transcription factor that controls various genes that are important for immunity and inflammation.17) NF-kB is mainly composed of p50 and p65. 17) In unstimulated cells, NF-kB is present in the cytoplasm through interactions with an inhibitory protein, IkB. NF-kB is activated by IkBa degradation following phosphorylation of IkBa. 18)Platycodi Radix is the root of Platycodon grandiflorum A. DE (Campanulaceae).19) It is edible and the principal herb in Oriental medicine for diseases of the lungs and throat, and is commonly used for the inflammatory conditions of the eyes, ears, and sinuses.19) Saponins (PS) are the primary constituents of Platycodi Radix, [20][21][22] and they are responsible for diverse effects including anti-inflammation, [23][24][25][26] anti-allergy, 23) anti-tumor, 27) augmentation of immune response, [28][29][30] and stimulating the apoptosis in skin cells. 27) In the last decade, PS has generated renewed interests due to their pharmacological potentials for healing the...

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“…In Korea, people usually gather bellflower roots in spring and autumn to use in seasoned salads or as a cooked potherb. In addition, because it is known to have a mucolytic and antitussive effect, Campanula punctata is used in Oriental medicine for the treatment of acute or chronic bronchitis, tonsillitis, and asthma [2].…”

Section: Introductionmentioning

confidence: 99%

Antinociception Effect and Mechanisms ofCampanula PunctataExtract in the Mouse

Park

Sim

Lim

et al. 2010

Korean J Physiol Pharmacol

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In the present study, the antinociceptive profiles of Campanula punctata extract were examined in ICR mice. The Campanula punctata contain a large dose of saponin. Campanula punctata extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, Campanula punctata extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P (0.7 μg) was diminished by Campanula punctata extract. Intraperitoneal (i.p.) pretreatment with yohimbine (α2-adrenergic receptor antagonist) attenuated antinociceptive effect induced by Campanula punctata extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by Campanula punctata extract in the writhing test. Our results suggest that Campanula punctata extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of Campanula punctata extract may be mediated by α2-adrenergic receptor, but not opioidergic and serotonergic receptors.

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Platycodin D and D3 Increase Airway Mucin Release in vivo and in vitro in Rats and Hamsters

Cited by 76 publications

References 17 publications

Platycodin D induces mitotic arrest in vitro, leading to endoreduplication, inhibition of proliferation and apoptosis in leukemia cells

Platycodin D induces mitotic arrest in vitro, leading to endoreduplication, inhibition of proliferation and apoptosis in leukemia cells

Anti-inflammatory Activity of Prosapogenin Methyl Ester of Platycodin D via Nuclear Factor-kappaB Pathway Inhibition

Antinociception Effect and Mechanisms ofCampanula PunctataExtract in the Mouse

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