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 ; Pei, Huijie ; He, Wei ; 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.

06 Nov 2024·Journal of Agricultural and Food Chemistry

Ginsenoside Rk3 Treats Corneal Injury Through the HMGB1/TLR4/NF-κB Pathway

Article

Author: Chen, Zhiqi ; Ma, Xiaoxuan ; He, Lei ; Liu, Yannan ; Qu, Linlin ; Fan, Daidi ; Huang, Yingcong ; Wu, Yuqing

The cornea serves as a vital protective shield for the eye, safeguarding its intricate internal structures from external threats. Damage to the cornea compromises this protective function, triggering inflammation and potentially causing long-term harm. While ginsenoside Rk3 has demonstrated potential for repairing the corneal barrier and reducing inflammation, its effectiveness in treating corneal damage remains relatively unexplored. This comprehensive study uses both in vivo and in vitro models to investigate the therapeutic capabilities of ginsenoside Rk3. Using two models of corneal damage, a benzalkonium chloride-induced mouse model and a high osmolarity-induced human corneal epithelial cell model, we scrutinized the effects of ginsenoside Rk3 treatment. Our results showed that ginsenoside Rk3-treated mice manifested reduced corneal damage and inflammation compared with their untreated counterparts. Furthermore, mice treated with ginsenoside Rk3 exhibited an organized arrangement of corneal cells and diminished stromal layer thickness, indicating reparative properties of ginsenoside Rk3. Additionally, ginsenoside Rk3 increased the expression of tight junction proteins, suppressed inflammatory factors, and decreased HMGB1 protein expression, thereby modulating downstream signaling pathways. Collectively, our findings present compelling evidence that ginsenoside Rk3 is a promising therapeutic option for corneal injury. By repairing the corneal barrier, mitigating inflammation, and modulating specific protein levels, ginsenoside Rk3 opens new avenues for managing corneal damage.

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 ; Xu, Xiaojun ; Shan, Ling ; Yang, Peng ; 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.

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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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