1,2-Dihydroxybenzene can induce spontaneous convulsive activity in the anaesthetized mouse and produce myoclonic jerks in the rat. It regulated 5-Hydroxytryptamine (5-HT) levels.
Coenzyme Q10, an essential cofactor of the electron transport chain, has neuroprotective effect in the cerebral ischemia via as a potent antioxidant and oxygen derived free radicals scavenger. Treatment with coenzyme Q10 in patients with myocardial infarction (MI) may be beneficial in patients with high risk of atherothrombosis. The coenzyme Q10 and alpha-lipoic acid supplementation can improve bladder function after outlet obstruction. The combination of Coenzyme Q10 and creatine may be useful in the treatment of neurodegenerative diseases such as Parkinson's disease and Huntington's Diseases. Coenzyme Q10 supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes, the mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress.
1. Celastrol has potential to be used as an antiangiogenesis drug through its role in suppressing VEGF receptors expression.
2. Celastrol has anti-proliferative activity, it has anti-tumor effect on various cancers.
3. Celastrol has anti-inflammatory activity, used for clinical treatment for rheumatoid arthritis.
4. Celastrol, a novel HSP90 inhibitor, can deplete Bcr–Abl and induce apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation.
5. Celastrol has antioxidant and anti-inflammatory activities and has effects on cognitive functions, suggest that the drug may be useful to treat accompanied by inflammation, such as Alzheimer's disease (AD) .
6.. Celastrol inhibits Plasmodium falciparum enoyl-acyl carrier protein reductase.
Trigonelline chloride, an alkaloid with potential antidiabetic activity, is present in considerable amounts in coffee. Trigonelline hydrochloride reduces diabetic auditory neuropathy by affecting β cell regeneration.
1. Harpagoside has anti-inflammatory effects, it blocks lipopolysaccharide (LPS)-induced bone loss in an inflammatory osteoporosis model, and it does not prevent ovariectomy-mediated bone erosion in a postmenopausal osteoporosis model.
2. Harpagoside dose-dependently inhibits LPS-stimulated NF-kappaB promoter activity in a gene reporter assay in RAW 264.7 cells, it suppresses lipopolysaccharide-induced iNOS and COX-2 expression through inhibition of NF-κB activation.
3. Harpagoside may lead to a partial prevention of obesity-induced atherosclerosis by attenuating inflammatory responses.
4. Harpagoside attenuates the MPTP/MPP + induced dopaminergic neurodegeneration and movement disorder mainly through elevating glial cell line-derived neurotrophic factor.
5. Harpagoside exerts neuroprotection effect and ameliorates learning and memory deficit appears to be associated, at least in part, with up-regulation of brain-derived neurotrophic factor (BDNF) content as well as activating its downstream signaling pathways, e.g., MAPK/PI3K pathways; it has potential to be a therapeutic agent against Alzheimer’s disease (AD).