Neuroprotective Effects of Water Extract from Brown Algae Petalonia binghamiae in an Experimental Model of Focal Cerebral Ischemia In Vitro and In Vivo

Author:

Eom Sun Ho1,Hong Geum-Lan2ORCID,Kang Hyun Bae1,Lee Nam-Seob2,Kim Do Kyung2ORCID,Jeong Young Gil2,Kim Chun-Sung3,Yoo Yung Choon4,Lee Bong Ho5,Jung Ju-Young6ORCID,Kim Dong-Sub7ORCID,Han Seung Yun2ORCID

Affiliation:

1. Healinnols Inc., Daejeon 34054, Republic of Korea

2. Department of Anatomy, College of Medicine, Konyang University, Daejeon 35365, Republic of Korea

3. Department of Oral Biochemistry, College of Dentistry, Chosun University, Gwangju 61452, Republic of Korea

4. Department of Microbiology, College of Medicine, Konyang University, Daejeon 35365, Republic of Korea

5. Department of Chemical Technology, Hanbat National University, Daejeon 34158, Republic of Korea

6. Department of Histology & Institute of Veterinary Science, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Republic of Korea

7. Division of Natural Product Research, Korea Prime Pharmacy Co., Ltd., Gwangju 61473, Republic of Korea

Abstract

Focal cerebral ischemia (fCI) can result in brain injury and sensorimotor deficits. Brown algae are currently garnering scientific attention as potential therapeutic candidates for fCI. This study investigated the therapeutic effects of the hot water extract of Petalonia binghamiae (wPB), a brown alga, in in vitro and in vivo models of fCI. The neuroprotective efficacy of wPB was evaluated in an in vitro excitotoxicity model established using HT-22 cells challenged with glutamate. Afterward, C57/BL6 mice were administered wPB for 7 days (10 or 100 mg/kg, intragastric) and subjected to middle cerebral artery occlusion and reperfusion (MCAO/R) operation, which was used as an in vivo fCI model. wPB co-incubation significantly inhibited cell death, oxidative stress, and apoptosis, as well as stimulated the expression of heme oxygenase-1 (HO-1), an antioxidant enzyme, and the nuclear translocation of its upstream regulator, nuclear factor erythroid 2-related factor 2 (Nrf2) in HT-22 cells challenged with glutamate-induced excitotoxicity. Pretreatment with either dose of wPB significantly attenuated infarction volume, neuronal death, and sensorimotor deficits in an in vivo fCI model. Furthermore, the attenuation of oxidative stress and apoptosis in the ischemic lesion accompanied the wPB-associated protection. This study suggests that wPB can counteract fCI via an antioxidative effect, upregulating the Nrf2/HO-1 pathway.

Funder

Ministry of Oceans and Fisheries, Korea

National Research Foundation, Korea

Publisher

MDPI AG

Subject

Microbiology (medical),Molecular Biology,General Medicine,Microbiology

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