Peimisine

Antiasthmatic mechanism of peimisine in Fritillaria monantha.[Reference: WebLink]

Chinese Traditional & Herbal Drugs, 2009, 40(4):597-601.

To approach the antiasthmatic mechanism of Peimisine in Fritillaria monatha.
METHODS AND RESULTS:
To observe the effect of Peimisine in the different concentration on the tracheal smooth muscle contraction in vitro organ induced by Ach, His, β-receptor, CaCl 2, Pro, in nitricoxide synthase catastaltica. Peimisine (0.046 and 0.092 mmol/L) made the EC 50 induced by Ach increased; The EC 50 of peimsine (0.092 mmol/L) was not changed by His; The EC 50 of Peimisine (0.092 mmol/L) was not significantly different to tracheal smooth muscle contraction induced by CaCl 2; Three dosages of Peimisine had significant inhibition on the release of intracellular calcium induced by CaCl 2 (P < 0.05, 0.01, and 0.001) in a dose-dependent manner. But extracellular calcium influx was not significantly inhibited. Comparing with the L-NAME+dissolvant group, three dosages of Peimisine couldn't restrain the contraction and had no significant difference.
CONCLUSIONS:
Peimisine could affect M-receptor, excit β-receptor, restrain the release of internal calcium, and promote to releaseing nitrogen monoxidum in order to relax tracheal smooth muscle and relieve asthma.

Peimisine attenuates acute lung injury induced by lipopolysaccharide in mice[Reference: WebLink]

Lishizhen Medicine & Materia Medica Research, 2014, 8(13-14):1842-7.

To determine the protective effect of Peimisine on acute lung injury( ALI) induced by lipopolysaccharide( LPS) and its protective mechanism mice.
METHODS AND RESULTS:
The mice were randomly allocated into sham,LPS and Peimisine + LPS groups. The ALI mice was induced by LPS after etherization. The Peimisine was injected by belly cavity 30 minutes prior to the LPS challenge,one time/d,3 times totally. The mice were killed 24h after the third Peimisine injection to observe the amount of LDH,MDA in plasma,the lung tissue pathology,the total protein,white blood cell and differential count in the bronchoalveolar lavage fluid( BALF). LDH,MDA amount in plasma,Lung tissue,and BALF showed serious inflammatory changes in the LPS group. Compared with the LPS group,Peimisine attenuates Lung tissue injury,LDH and MDA amount in ALI mice in a dose dependent manner. Peimisine( 0. 12mg) lowered the total protein,total white blood cells,lymphocyte and neutrophilic leukocyte in BALF compared with the LPS group.
CONCLUSIONS:
Peimisine can play a protective role against LPS-induced acute lung injury.

Protection of peimisine on hepatic fibrosis of rats induced by CCl4.[Reference: WebLink]

Chinese Traditional & Herbal Drugs, 2013, 44(11):1455-9.

To investigate the protective effect of Peimisine on carbon tetrachloride(CCl4)-induced hepatic fibrosis in rats.
METHODS AND RESULTS:
The rats were divided into control,model,low-,mid-,and high-dose(2.5,5,and 10 mg/kg) Peimisine groups.Hepatic fibrosis models were induced by ip injection of CCl4 in rats once every 3 d for 8 weeks.The rats in the treatment groups were administered four weeks after the model establishment,once daily until the end of the week 4 after the model establishment.The levels of serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),alkaline phosphatase(ALP),glutamyl transpeptidasecc(GGT),hyaluronie acid(HA),laminin(LN),type III procollagenc(PC-III),and collegen type IV(IV-C) were assayed,and hepatic tissue contents of hydroxyprolinc(Hyp),superoxide dismutase(SOD),and malondialdehyde(MDA) were determined.The effect of Peimisine on hepatic fibrosis in rats was observed. Compared with the model control group,the hepatic fibrosis of rats in Peimisine groups was improved obviously,the levels of ALT,AST,ALP,and GGT in serum were lowered obviously(P 0.05,0.01),also the serum levels of HA,LN,PC-III,IV-C,and the contents of Hyp and MDA in liver tissue were decreased(P 0.01),while the level of SOD was increased(P 0.01).
CONCLUSIONS:
Peimisine has the protective effect on the experimental hepatic fibrosis formation.The possible mechanisms are associated with inhibiting fibrogenesis and fibrosis accumulation,and decreasing lipid peroxidation.

Planta Med. 2003 Jun;69(6):564-5.

Angiotensin converting enzyme (ACE) inhibitory alkaloids from Fritillaria ussuriensis.[Pubmed: 12865981 ]

Bioassay-guided fractionation of the BuOH-soluble extract of Fritillaria ussuriensis afforded verticinone ( 1), verticine ( 2), and Peimisine ( 3). Purification of these compounds was achieved with the use of various chromatographic methods.
METHODS AND RESULTS:
The structures of the compounds were identified on the basis of MS and NMR data analysis. Compounds 1 - 3 inhibited angiotensin I converting enzyme activity in a dose-dependent manner, displaying 50 % inhibitory concentration values of 165.0 microM, 312.8 microM, 526.5 microM, respectively.
CONCLUSIONS:
The presence of these active substances may be responsible, at least in part, for the antihypertensive action of the bulbs of Fritillaria ussuriensis.