Acetylshikonin (50 mg/kg; Intraperitoneal injection; Three times per week for 6 weeks) significantly inhibited tumor growth in BALB/c nude mice in a concentration-dependent manner[6].
Acetylshikonin (270-1080 mg/kg; Intragastric administration; Once a day for 30 days) reduces D-galactose-induced (150 mg/kg) cognitive impairment and hippohippoal aging by reducing oxidative stress and neuroinflammation and inhibiting the activation of the p53/p21 signaling pathway in mice[1].
Acetylshikonin (2 mg/kg; Intramuscular injection; Single dose) inhibits Coxsackievirus A16 (CVA16) replication in mice[2].
Acetylshikonin (100 mg/kg; Intragastric administration; Once a day for eight weeks) inhibits renal fibrosis by inhibiting TGF-β1/Smad pathway without affecting blood glucose, thus reducing the damage of renal function in streptozotocin (STZ) -induced diabetic C57BL/6 mice[5].
Acetylshikonin (10 mk/kg; Intraperitoneal injection; Once a day for three days) reduces alloxouracil- (180 mg/kg; Intraperitoneal injection; Single dose) induced blood glucose level in diabetic mice[3].
Acetylshikonin (540 mg/kg; Oral administration; Once a day for eight weeks) reduces liver fat accumulation by regulating fat metabolism and liver inflammation in obese C57BL/6J mice, thereby improving obesity and nonalcoholic fatty liver disease (NAFLD)[4].
Acetylshikonin (120-1080 mg/kg; Intragastric administration;) doesn’t affect the ability of pregnancy in Sprague-Dawley rats at low doses (120 mg/kg and 360 mg/kg), but inhibits the ability of pregnancy in Sprague-Dawley rats at high doses (1080 mg/kg) by affecting the secretion of gonadotropin (GTH) and reducing the levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH)[7].
| Animal Model: | D-galactose (D-gal)-induced sub-acuteaging mouse model of Alzheimer’s disease (AD)[1] |
| Dosage: | 270 mg/kg, 540 mg/kg, 1080 mg/kg |
| Administration: | Intragastrical administration (i.g.); Once daily for 30 days. After D-gal treatment (150 mg/kg; Subcutaneous injection (s.c.); Once daily for 30 days) |
| Result: | Decreased levels of the pro-inflammatory cytokines IL-1β and TNF-α.
Decreased the content of MDA and increased the activity of SOD.
Significantly mitigated D-Gal-induced downregulation of SIRT1 in hippocampal neurons.
Significantly inhibited the expression of p53, acetyl-p53, and p21 in mice (all proteins associated with hippocampal aging).
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| Animal Model: | CAV16-indeced ICR suckling mice model[2] |
| Dosage: | 2 mg/kg |
| Administration: | Intramuscular injection (i.m.); Single dose. After CVA16 treatment (10[5.5] TCID50/g; Intramuscular injection (i.m.); Single dose ) |
| Result: | Delayed death of the mice (6 days post-infection and 7 dpi), and eventually resulted in a survival rate of 50% and 70% for the mice in the treatment and prevention groups, respectively (the death of the control mice began at 4 days after infection and all died at 6 days after infection).
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| Animal Model: | Obese male C57BL/6J Mice model[4] |
| Dosage: | 540 mg/kg |
| Administration: | Oral gavage (P.O.); Once daily for 8 weeks |
| Result: | Reduced body mass index (BMI) and food efficiency in obese mice by 17.1% and 48.2%, respectively.
Decreased plasma glucose, CHE, AST and ALT levels by 34.1%, 45.5% and 27.2%, respectively.
Significantly inhibited the levels of serum proinflammatory cytokines TNF-α, IL-6 and IL-1β by 49.1%, 41.1% and 45.6%, respectively.
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