Andrographolide does not protect against neuroinflammation in a Parkinsonism model: Focus on tumor necrosis factor alpha

The incidence of Parkinson's disease has increased in recent years, with pathological theories newly emerging. One of the most acknowledged theories is the neuroinflammation theory, which involves microglial activation and the expression of proinflammatory cytokines. Previous studies have confirmed the effects of andrographolide on anti-inflammatory characteristics; however, the role of andrographolide as a neuroprotective agent in 1-methyl-4-phenyl-1,2,3,4-tetrahydropiridine (MPTP)-induced Parkinsonism remains unknown. In this study, we used several doses of andrographolide and investigated its potential as a neuroprotective agent in an MPTP-induced Parkinsonism model. Five types of treatment were used for five groups of C57BL/6 mice. These treatments included (1) normal control, (2) MPTP treated, (3) MPTP and selegiline treated, (4) andrographolide treated at 5 mg/kgbw, and (5) andrographolide treated at 50 mg/kgbw. Immunohistochemical analyses were performed to determine tumor necrosis factor-alpha (TNFα) levels. No significant differences were observed in TNFα levels between control groups and those treated with andrographolide. TNFα levels were determined to be 10.0 ± 3.5 for the normal group, 8.4 ± 2.9 for the selegiline-treated group, 12.8 ± 7.8 for the MPTP-treated group, 5.4 ± 2.4 for the andrographolide-treated group at 50 mg/kgbw, and 5.8 ± 1.6 for the andrographolide-treated group at 5 mg/kgbw. This study suggests that no significant reduction of TNFα levels occur after treatment with andrographolide at doses of 5 and 50 mg/kgbw in an MPTP-treated Parkinsonism model, indicating no neuroprotective effect of andrographolide.