Journal: Neural Regeneration Research

Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

doi: 10.4103/NRR.NRR-D-23-01511

Figure Lengend Snippet: Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

Article Snippet: The rotarod test was performed using a five-lane rotarod apparatus (Jinan Yiyan Technology Development Co., Ltd, Jinan, China, YLS-4C) as described previously (Kumar et al., 2013), with some modifications.

Techniques: Control, Expressing, Western Blot, Immunofluorescence, Staining, Tandem Mass Spectroscopy

Journal: Neural Regeneration Research

Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

doi: 10.4103/NRR.NRR-D-23-01511

Figure Lengend Snippet: Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

Article Snippet: The rotarod test was performed using a five-lane rotarod apparatus (Jinan Yiyan Technology Development Co., Ltd, Jinan, China, YLS-4C) as described previously (Kumar et al., 2013), with some modifications.

Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Phospho-proteomics, Real-time Polymerase Chain Reaction

Journal: Redox Biology

Article Title: Mitochondria-targeted therapy with metformin and MitoQ reduces oxidative stress, improves mitochondrial function, and restores metabolic homeostasis in a murine model of Gulf War Illness

doi: 10.1016/j.redox.2025.103714

Figure Lengend Snippet: The effect of m etformin and MitoQ on behavioral signs in mice exposed to PB/PER. (A) Schematic representation of Gulf War Illness study using C57BL/6 mice (B) Body weight of mice during PB/PER injection period, n = 49 (10 and 39); vehicle (Veh) = DMSO. Multiple t -test used for p value; ∗p < 0.05 (C) Body weight of mice before (at the end of 8 months post-PB/PER exposure) and after the 8-week treatment (oral) with vehicle (distilled water), metformin and/or MitoQ. The treatment was for 2 months. Tx = treatment with vehicle, metformin and/or MitoQ. One way ANOVA was used to calculate significance. The graphs are shown as individual data points along with Mean ± SEM. n = 4-19. (D – F) Behavior analysis (D) Hanging wire test (E) Rotarod test, and (F) Behavior tests using Noldus Phenotyper. See the original data in . The experiment was conducted in two batches, with all groups tested in each batch. The graphs are shown as individual data points along with Mean ± SEM. n = 8–10, One-way ANOVA was used for analysis. ∗p < 0.05,∗∗p < 0.01.

Article Snippet: The graphs are shown as individual data points along with Mean ± SEM. n = 4-19. (D – F) Behavior analysis (D) Hanging wire test (E) Rotarod test, and (F) Behavior tests using Noldus Phenotyper.

Techniques: Injection