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Figure legends
Figure 1. The schedule used in this study.
Figure 2. Luteolin protects against LPS-induced neuronal injury
in the nigrostriatal system of the PD mouse model. (A) Representative
immunohistochemical staining for tyrosine hydroxylase in the SN. Scale
bar = 100μm. (B) Number of Th-positive cells within the SN was counted.
(B) Abundance of DA, DOPAC, and HVA in the striatum measured by
LC-MS/MS. N = 5 per group. **p < 0.01, ***p< 0.001 compared to the sham group. #p <
0.05, ##p < 0.01 compared to the LPS group.
Figure 3. Luteolin improved motor performance in the PD model.(A) In the pole test, the time for each mouse to completely turn its
head downward (T-turn) and climb down to the ground (T-D) was recorded.
(B) Using a rotarod test, the latency to fall off the rotating rod was
recorded. N = 10 per group.
***p < 0.001
compared to the sham group, #p < 0.05, ##p< 0.01 compared to the LPS group.
Figure 4. Luteolin shifted microglial M1/M2 polarization and
inhibited pro-inflammatory cytokine release in the PD model. (A)
Relative mRNA expression of microglial M2 polarization phenotypic
markers Arg-1, CD206, and IL-10. (B) Relative mRNA expression of
microglial M1 polarization markers CD32, iNOS, and TNF-α. (C) Relative
mRNA expression of IBA-1. (D) Pro-inflammatory cytokine levels in the
mesencephalic tissue were measured using ELISA. N = 5 per group.
***p < 0.001 compared to the sham group; # p< 0.05, ##p < 0.01 compared to the LPS-only
group.
Figure 5. Luteolin shifts microglial M1/M2 polarization and
inhibited pro-inflammatory cytokine release in BV2 microglia cells
challenged with LPS. (A) Relative mRNA expression of microglial M2
phenotypic markers Arg-1, CD206, and IL-10. (B) Relative mRNA expression
of microglial M1 phenotypic markers CD32, iNOS, and TNF-α. (C) Relative
mRNA expression of IBA-1. (D) Pro-inflammatory cytokines levels in BV2
cells were measured using ELISA. N = 5 per group. ***p< 0.001, **p < 0.01 compared to the Control
(sham) group, #p < 0.05, ##p < 0.01
compared to the LPS-only group.
Figure 6. Luteolin pretreatment before LPS challenging in BV2
rescued neuronal injury in the co-cultured system. (A) A sketch of the
co-culture system used. (B) Apoptosis detected by flow cytometry. (C)
Bar graph showing the cellular apoptosis. (D) Cell viability was
measured by CCK8. N = 4 per group. ***p < 0.001
compared to the control group, #p < 0.05, ##p< 0.01 compared to the LPS-only group.
Figure 7. Luteolin treatment reduces LPS-induced TLR4/NFkB
signaling in vivo and in vitro model systems. (A)
Relative TLR4 mRNA expression in mesencephalic tissue dissected from
mice in the indicated treatment groups. N = 5 measurements per group.
(B) Relative TLR4 mRNA abundance in cultured BV2. N = 5 measurements per
group. (C) Representative immunofluorescent confocal images of TLR4
staining in BV2 cells. Scale bar = 20 μm. (D) Mean TLR4 fluorescence
intensity in treated and untreated BV2 cells. N = 5 measurements per
group. (E) Immunoblots (top ) and bar graph of immunoblot
quantification (bottom ) for TLR4 in mesencephalic tissue. N = 3
per group. (F) Immunoblots (top ) and bar graph of immunoblot
quantification (bottom ) for TLR4 in treated and untreated BV2
cells. N = 3 per group. (G) Immunoblots (top ) and bar graph of
immunoblot quantification (bottom ) for phospho-p65 in
mesencephalic tissue. N = 3 per group. (H) Immunoblots (top ) and
bar graph of immunoblot quantification (bottom ) for phospho-p65
in treated and untreated BV2 cells. N = 3 per group. ***p< 0.001 compared to the control group, #p <
0.05, ##p < 0.01 compared to the LPS-only group.