Minocycline Treatment in SOD1 G93A Mice
Objective: To assess the therapeutic effects of minocycline treatment on disease progression in SOD1 G93A transgenic mice
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Materials1
Nichi-iko Pharmaceutical Co. Ltd. • not applicable • not specified • not specified
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Protocol Steps
Animal acquisition and genotyping
SOD1 G93A transgenic mice (B6.Cg-Tg [SOD1-G93A] 1Gur/J line) were purchased from Jackson Laboratory. Maintenance and genotyping protocols were performed according to previously described methods.
Note: Mice were obtained from Jackson Laboratory (Bar Harbor, ME, USA)
View evidence from paper
“SOD1 G93A transgenic mice, which carry the G93A mutant form of the human SOD1 (B6.Cg-Tg [SOD1-G93A] 1Gur/J line), were purchased from the Jackson Laboratory”
Random group assignment
Transgenic mice were randomly divided into two groups: minocycline hydrochloride-treated group and untreated control group
Note: Randomization method not specified
View evidence from paper
“The transgenic mice were randomly divided into minocycline hydrochloride (Nichi-iko Pharmacceutical Co. Ltd., Toyama, Japan)-treated and untreated groups”
Minocycline administration initiation
Minocycline hydrochloride treatment was initiated at 8 weeks after birth
Note: Treatment continued until end stage of disease
View evidence from paper
“Minocycline (33 mg/kg) was administered intraperitoneally five times a week from 8 weeks after birth to end stage”
Intraperitoneal minocycline administration
Minocycline was administered via intraperitoneal injection at a dose of 33 mg/kg, five times per week
Note: Route of administration: intraperitoneal; Frequency: 5 times per week; Dose: 33 mg/kg
View evidence from paper
“Minocycline (33 mg/kg) was administered intraperitoneally five times a week from 8 weeks after birth to end stage”