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Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish. / Nie, Yingying; Yang, Jingming; Zhou, Longjian; Yang, Zhiyou; Liang, Jinyue; Liu, Yayue; Ma, Xiaoxiang; Qian, Zhongji; Hong, Pengzhi; Kalueff, Allan V.; Song, Cai; Zhang, Yi.

In: Journal of Neuroinflammation, Vol. 19, No. 1, 39, 12.2022.

Research output: Contribution to journalArticlepeer-review

Harvard

Nie, Y, Yang, J, Zhou, L, Yang, Z, Liang, J, Liu, Y, Ma, X, Qian, Z, Hong, P, Kalueff, AV, Song, C & Zhang, Y 2022, 'Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish', Journal of Neuroinflammation, vol. 19, no. 1, 39. https://doi.org/10.1186/s12974-022-02403-3

APA

Nie, Y., Yang, J., Zhou, L., Yang, Z., Liang, J., Liu, Y., Ma, X., Qian, Z., Hong, P., Kalueff, A. V., Song, C., & Zhang, Y. (2022). Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish. Journal of Neuroinflammation, 19(1), [39]. https://doi.org/10.1186/s12974-022-02403-3

Vancouver

Author

Nie, Yingying ; Yang, Jingming ; Zhou, Longjian ; Yang, Zhiyou ; Liang, Jinyue ; Liu, Yayue ; Ma, Xiaoxiang ; Qian, Zhongji ; Hong, Pengzhi ; Kalueff, Allan V. ; Song, Cai ; Zhang, Yi. / Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish. In: Journal of Neuroinflammation. 2022 ; Vol. 19, No. 1.

BibTeX

@article{d643b8e0c5ca4e9599930d1d06936c97,
title = "Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish",
abstract = "Background: Mounting evidences indicate that oxidative stress, neuroinflammation, and dysregulation of gut microbiota are related to neurodegenerative disorders (NDs). Butyrolactone I (BTL-I), a marine fungal metabolite, was previously reported as an in vitro neuroprotectant and inflammation inhibitor. However, little is known regarding its in vivo effects, whereas zebrafish (Danio rerio) could be used as a convenient in vivo model of toxicology and central nervous system (CNS) diseases. Methods: Here, we employed in vivo and in silico methods to investigate the anti-NDs potential of BTL-I. Specifically, we established a cognitive deficit model in zebrafish by intraperitoneal (i.p.) injection of aluminum trichloride (AlCl3) (21 μg) and assessed their behaviors in the T-maze test. The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) as well as acetylcholinesterase (AChE) activity or glutathione (GSH) levels were assayed 24 h after AlCl3 injection. The intestinal flora variation of the zebrafish was investigated by 16S rDNA high-throughput analysis. The marine fungal metabolite, butyrolactone I (BTL-I), was used to modulate zebrafish cognitive deficits evoked by AlCl3 and evaluated about its effects on the above inflammatory, cholinergic, oxidative stress, and gut floral indicators. Furthermore, the absorption, distribution, metabolism, excretion, and toxicity (ADMET) and drug-likeness properties of BTL-I were studied by the in silico tool ADMETlab. Results: BTL-I dose-dependently ameliorated AlCl3-induced cognitive deficits in zebrafish. While AlCl3 treatment elevated the levels of central and peripheral proinflammatory cytokines, increased AChE activity, and lowered GSH in the brains of zebrafish, these effects, except GSH reduction, were reversed by 25–100 mg/kg BTL-I administration. Besides, 16S rDNA high-throughput sequencing of the intestinal flora of zebrafish showed that AlCl3 decreased Gram-positive bacteria and increased proinflammatory Gram-negative bacteria, while BTL-I contributed to maintaining the predominance of beneficial Gram-positive bacteria. Moreover, the in silico analysis indicated that BTL-I exhibits acceptable drug-likeness and ADMET profiles. Conclusions: The present findings suggest that BTL-I is a potential therapeutic agent for preventing CNS deficits caused by inflammation, neurotoxicity, and gut flora imbalance.",
keywords = "Acetylcholinesterase, Butyrolactone I, Inflammation, Intestinal flora, Neurodegenerative diseases, Oxidative stress, Zebrafish/metabolism, Oxidative Stress, Acetylcholinesterase/metabolism, Inflammation/chemically induced, Gastrointestinal Microbiome, Cognition, 4-Butyrolactone/analogs & derivatives, Aluminum Chloride/toxicity, Animals",
author = "Yingying Nie and Jingming Yang and Longjian Zhou and Zhiyou Yang and Jinyue Liang and Yayue Liu and Xiaoxiang Ma and Zhongji Qian and Pengzhi Hong and Kalueff, {Allan V.} and Cai Song and Yi Zhang",
note = "Publisher Copyright: {\textcopyright} 2022, The Author(s).",
year = "2022",
month = dec,
doi = "10.1186/s12974-022-02403-3",
language = "English",
volume = "19",
journal = "Journal of Neuroinflammation",
issn = "1742-2094",
publisher = "BioMed Central Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish

AU - Nie, Yingying

AU - Yang, Jingming

AU - Zhou, Longjian

AU - Yang, Zhiyou

AU - Liang, Jinyue

AU - Liu, Yayue

AU - Ma, Xiaoxiang

AU - Qian, Zhongji

AU - Hong, Pengzhi

AU - Kalueff, Allan V.

AU - Song, Cai

AU - Zhang, Yi

N1 - Publisher Copyright: © 2022, The Author(s).

PY - 2022/12

Y1 - 2022/12

N2 - Background: Mounting evidences indicate that oxidative stress, neuroinflammation, and dysregulation of gut microbiota are related to neurodegenerative disorders (NDs). Butyrolactone I (BTL-I), a marine fungal metabolite, was previously reported as an in vitro neuroprotectant and inflammation inhibitor. However, little is known regarding its in vivo effects, whereas zebrafish (Danio rerio) could be used as a convenient in vivo model of toxicology and central nervous system (CNS) diseases. Methods: Here, we employed in vivo and in silico methods to investigate the anti-NDs potential of BTL-I. Specifically, we established a cognitive deficit model in zebrafish by intraperitoneal (i.p.) injection of aluminum trichloride (AlCl3) (21 μg) and assessed their behaviors in the T-maze test. The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) as well as acetylcholinesterase (AChE) activity or glutathione (GSH) levels were assayed 24 h after AlCl3 injection. The intestinal flora variation of the zebrafish was investigated by 16S rDNA high-throughput analysis. The marine fungal metabolite, butyrolactone I (BTL-I), was used to modulate zebrafish cognitive deficits evoked by AlCl3 and evaluated about its effects on the above inflammatory, cholinergic, oxidative stress, and gut floral indicators. Furthermore, the absorption, distribution, metabolism, excretion, and toxicity (ADMET) and drug-likeness properties of BTL-I were studied by the in silico tool ADMETlab. Results: BTL-I dose-dependently ameliorated AlCl3-induced cognitive deficits in zebrafish. While AlCl3 treatment elevated the levels of central and peripheral proinflammatory cytokines, increased AChE activity, and lowered GSH in the brains of zebrafish, these effects, except GSH reduction, were reversed by 25–100 mg/kg BTL-I administration. Besides, 16S rDNA high-throughput sequencing of the intestinal flora of zebrafish showed that AlCl3 decreased Gram-positive bacteria and increased proinflammatory Gram-negative bacteria, while BTL-I contributed to maintaining the predominance of beneficial Gram-positive bacteria. Moreover, the in silico analysis indicated that BTL-I exhibits acceptable drug-likeness and ADMET profiles. Conclusions: The present findings suggest that BTL-I is a potential therapeutic agent for preventing CNS deficits caused by inflammation, neurotoxicity, and gut flora imbalance.

AB - Background: Mounting evidences indicate that oxidative stress, neuroinflammation, and dysregulation of gut microbiota are related to neurodegenerative disorders (NDs). Butyrolactone I (BTL-I), a marine fungal metabolite, was previously reported as an in vitro neuroprotectant and inflammation inhibitor. However, little is known regarding its in vivo effects, whereas zebrafish (Danio rerio) could be used as a convenient in vivo model of toxicology and central nervous system (CNS) diseases. Methods: Here, we employed in vivo and in silico methods to investigate the anti-NDs potential of BTL-I. Specifically, we established a cognitive deficit model in zebrafish by intraperitoneal (i.p.) injection of aluminum trichloride (AlCl3) (21 μg) and assessed their behaviors in the T-maze test. The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) as well as acetylcholinesterase (AChE) activity or glutathione (GSH) levels were assayed 24 h after AlCl3 injection. The intestinal flora variation of the zebrafish was investigated by 16S rDNA high-throughput analysis. The marine fungal metabolite, butyrolactone I (BTL-I), was used to modulate zebrafish cognitive deficits evoked by AlCl3 and evaluated about its effects on the above inflammatory, cholinergic, oxidative stress, and gut floral indicators. Furthermore, the absorption, distribution, metabolism, excretion, and toxicity (ADMET) and drug-likeness properties of BTL-I were studied by the in silico tool ADMETlab. Results: BTL-I dose-dependently ameliorated AlCl3-induced cognitive deficits in zebrafish. While AlCl3 treatment elevated the levels of central and peripheral proinflammatory cytokines, increased AChE activity, and lowered GSH in the brains of zebrafish, these effects, except GSH reduction, were reversed by 25–100 mg/kg BTL-I administration. Besides, 16S rDNA high-throughput sequencing of the intestinal flora of zebrafish showed that AlCl3 decreased Gram-positive bacteria and increased proinflammatory Gram-negative bacteria, while BTL-I contributed to maintaining the predominance of beneficial Gram-positive bacteria. Moreover, the in silico analysis indicated that BTL-I exhibits acceptable drug-likeness and ADMET profiles. Conclusions: The present findings suggest that BTL-I is a potential therapeutic agent for preventing CNS deficits caused by inflammation, neurotoxicity, and gut flora imbalance.

KW - Acetylcholinesterase

KW - Butyrolactone I

KW - Inflammation

KW - Intestinal flora

KW - Neurodegenerative diseases

KW - Oxidative stress

KW - Zebrafish/metabolism

KW - Oxidative Stress

KW - Acetylcholinesterase/metabolism

KW - Inflammation/chemically induced

KW - Gastrointestinal Microbiome

KW - Cognition

KW - 4-Butyrolactone/analogs & derivatives

KW - Aluminum Chloride/toxicity

KW - Animals

UR - http://www.scopus.com/inward/record.url?scp=85124741897&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/1901b564-1b30-331b-9101-1e96fcfdc1ce/

U2 - 10.1186/s12974-022-02403-3

DO - 10.1186/s12974-022-02403-3

M3 - Article

C2 - 35130930

AN - SCOPUS:85124741897

VL - 19

JO - Journal of Neuroinflammation

JF - Journal of Neuroinflammation

SN - 1742-2094

IS - 1

M1 - 39

ER -

ID: 95284920