1. Tripdiolide has cytotoxic activity.
2. Tripdiolide has anti-rheumatic activity, suppresses pro-inflammatory gene expression, may be effective therapy for lupus nephritis.
1. Hypaconitine (HA), an active and highly toxic constituent derived from Aconitum species, is widely used to treat rheumatism, the hepatic cytochrome P450-catalyzed metabolism of HA.
2. Hypaconitine and aconitine produce neuromuscular blockade by reducing the evoked quantal release, the mechanism of this effect was attributed mainly to blocking of the nerve compound action potential.
3. Hypaconitine induces QT prolongation, mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs.
4. Hypaconitine has anti-inflammatory activity.
5. Hypaconitine can inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin can interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.
1. Sinomenine has anti-inflammatory and immunosuppressive effects, it can attenuate 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice and the therapeutic mechanism may be related to the reduction of up-regulated colonic TNF-alpha and IFN-gamma production caused by TNBS.
2. Sinomenine exerts anti- rheumatoid arthritis action probably through modulating the frequencies of Treg cells and Th17 cells in intestinal lymph nodes and yielding a trafficking of lymphocytes (especially Treg cells) from gut to joint.
3. Sinomenine plays the protective effects through inhibition of microglial inflammation, and the findings also provides a novel therapy to treat ICH induced brain injury.
4. Sinomenine has anti-inflammatory and neuroprotective activities through inhibition of microglial NADPH oxidase.
5. Sinomenine can prevent galactosamine (GalN)/lipopolysaccharide (LPS) -treated hepatic failure by suppressing TNF production and/or reactive oxygen generation.
1. Swertiamarin possesses anti-hyperglycemic, anti-hyperlipidemic, anti-diabetic activity and enhances β cell regeneration which causes reversal of diabetes.
2. Swertiamarin possesses significant antioxidant and hepatoprotective properties against d-GalN induced hepatotoxicity given at 100 and 200 mg/kg body weight orally for 8 days, which might be due to its in vitro antioxidant activity.
3. Swertiamarine has wound healing activity via the stimulation of collagen production and its mitotic activity, it also exhibits cytoprotective effects.
4. Swertiamarin can significantly increase high-density lipoprotein (HDL) levels and it shows a significant lipid-lowering effect, as well as a high antiatherogenic potential, overall swertiamarin is an effective lipid-lowering lead compound and can be useful for preventing atherosclerosis.
5. Swertiamarin possesses both peripheral and central antinociceptive activity.
6. Swertiamarin has anti-inflammatory activity, it inhibits the development of arthritis by modulating NF-κB/IκB and JAK2/STAT3 signaling, suggests that swertiamarin acts as an anti-rheumatic agent.
7. Swertiamarin has anti-diabetic effects, the anti-diabetic effect of swertiamarin is due to gentianine, an active metabolite of swertiamarin.
8. Swertiamarin stimulates gastric emptying and gastrointestinal motility by inhibiting the dopamine D2 receptor.
1. Bullatine A possesses anti-rheumatic, anti-inflammatory and anti-nociceptive effects, may be used for the treatment of neurodegenerative diseases such as arthritis.
2. Bullatine A produces antinociception without induction of tolerance and inhibits morphine antinociceptive tolerance, and provide pharmacological basis for concurrent bullatine A and morphine treatment for chronic pain and morphine analgesic tolerance.
3. Bullatine A stimulates spinal microglial dynorphin A expression to produce anti-hypersensitivity in a variety of rat pain models.