Characterization of ornithine decarboxylase with histidine decarboxylase activity in natural histidine decarboxylase gene deletion Enterobacter hormaechei RH3

Article

Author: Zou, Likou ; Yang, Yong ; Ma, Yixuan ; Li, Shuhong ; Ao, Xiaolin ; Hu, Kaidi ; Zhang, Yue ; He, Wei ; Pei, Huijie ; Liu, Aiping ; Hu, Xinjie ; Wang, Yilun ; Li, Jinhai ; Teng, Hui ; Li, Ran ; Yang, Lamei ; Liu, Shuliang ; Li, Jianlong ; Li, Qin

Histamine is predominantly produced in sausages via the decarboxylation of histidine by bacteria. Furthermore, histamine-producing bacteria usually possess the enzyme histidine decarboxylase (hdc). Enterobacter hormaechei RH3 isolated from sausages exhibited significant levels of histamine production despite the absence of hdc. In this study, we elucidated the previously unidentified mechanism underlying histamine production by RH3. We identified an enzyme, NehdX-772, exhibiting the hdc activity from the cell lysate supernatant of RH3, which was annotated as ornithine decarboxylase. The optimal activity of NehdX-772 was recorded at 35 °C and pH 6.0, and it could tolerate a salt concentration of 2.5% (w/v) NaCl. Moreover, artificial inoculation revealed that NehdX-772 was synthesized at significant levels in sausages, leading to an increase in histamine levels. The discovery of NehdX-772 explains the underlying mechanism of histamine production by RH3 and can be applied to decrease histamine production in sausages.

01 Oct 2024·Advanced Science

Ginsenoside Rg3 Restores Mitochondrial Cardiolipin Homeostasis via GRB2 to Prevent Parkinson's Disease

Article

Author: Qian, Cheng ; Cui, Qinghua ; Peng, Chao ; Yang, Sen ; Fang, Qiuyuan ; Li, Ping ; Shan, Ling ; Yang, Peng ; Xu, Xiaojun ; Qi, Li‐Feng‐Rong ; Wu, Ping ; Hua, Qian ; Ye, Cunqi ; Liu, Yuci ; Liu, Shuai ; Yang, Wei

AbstractRegulating cardiolipin to maintain mitochondrial homeostasis is a promising strategy for addressing Parkinson's disease (PD). Through a comprehensive screening and validation process involving multiple models, ginsenoside Rg3 (Rg3) as a compound capable of enhancing cardiolipin levels is identified. This augmentation in cardiolipin levels fosters mitochondrial homeostasis by bolstering mitochondrial unfolded protein response, promoting mitophagy, and enhancing mitochondrial oxidative phosphorylation. Consequently, this cascade enhances the survival of tyrosine hydroxylase positive (TH+) dopaminergic neurons, leading to an amelioration in motor performance within PD mouse models. Using limited proteolysis–small‐molecule mapping combined with molecular docking analysis, it has confirmed Growth Factor Receptor‐Bound Protein 2 (GRB2) as a molecular target for Rg3. Furthermore, these investigations reveal that Rg3 facilitates the interaction between GRB2 and TRKA (Neurotrophic Tyrosine Kinase, Receptor, Type 1), thus promotes EVI1 (Ecotropic Virus Integration Site 1 Protein Homolog) phosphorylation by ERK, subsequently increases CRLS1 (Cardiolipin Synthase 1) gene expression and boosts cardiolipin synthesis. The absence of GRB2 or CRLS1 significantly attenuates the beneficial effects of Rg3 on PD symptoms. Finally, Tenofovir Disoproxil Fumarate (TDF) that also promotes the binding between GRB2 and TRKA is further identified. The identified compounds, Rg3 and TDF, exhibit promising potential for the prevention of PD by bolstering cardiolipin expression and reinstating mitochondrial homeostasis.

01 Sep 2024·Cell Biology International

Ginsenoside Rb3 alleviates the formation of osteoclasts induced by periodontal ligament fibroblasts in the periodontitis microenvironment through the STAT3 pathway

Article

Author: Zhang, Yuhua ; Shi, Hanping

AbstractThis study explores the potential role and mechanism of Ginsenoside Rb3 (Rb3) in modulating osteoclastogenesis induced by human periodontal ligament fibroblasts (hPLFs) within the periodontitis microenvironment. We investigated the anti‐inflammatory effects of Rb3 on hPLFs stimulated with Porphyromonas gingivalis lipopolysaccharide (P.g‐LPS) utilizing quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assay techniques. Moreover, the functional role of Rb3 in hPLFs‐induced osteoclast formation was assessed by treating human bone marrow‐derived macrophages (hBMMs) with conditioned medium from hPLFs, followed by analyses through qPCR, western blot analysis, and staining for tartrate‐resistant acid phosphatase (TRAP) and phalloidin. The impact of Rb3 on the activation of the STAT3 signaling pathway was determined via western blot analysis. Results indicated that Rb3 treatment significantly suppressed the upregulation of pro‐inflammatory cytokines (TNF‐α, IL‐1β, IL‐6, MCP‐1, and IL‐18) at both gene and protein levels in hPLFs induced by P.g‐LPS. Furthermore, conditioned medium from Rb3 plus P.g‐LPS treated hPLFs notably decreased the number of TRAP‐positive cells, actin ring formations, and the expression of osteoclast marker genes (including CTSK, NFATC1, and ACP5). Rb3 also inhibited the P.g‐LPS‐induced activation of the STAT3 pathway, with the activation of STAT3 partially reversing the effects of Rb3 on inflammation and osteoclast differentiation. Collectively, Rb3 ameliorates inflammation in P.g‐LPS‐stimulated hPLFs and reduces hPLFs‐induced osteoclastogenesis by inhibiting the STAT3 signaling pathway, suggesting its potential as a therapeutic agent for periodontitis.

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Indication	Highest Phase	Country/Location	Organization	Date
Hepatocellular Carcinoma	Preclinical	KR	KIST Corp. (South Korea)	22 Mar 2024

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