Tyrosinase is a key enzyme in post-harvest browning of fruit and vegetable. To control and inhibit its activity is the most effective method for delaying the browning and extend the shelf life. In this paper, the inhibitory kinetics of 4-hydroxy cinnamic acid on mushroom tyrosinase was investigated using the kinetics method of substrate reaction. The results showed that the inhibition of tyrosinase by 4-hydroxy cinnamic acid was a slow, reversible reaction with fractional remaining activity. The microscopic rate constants were determined for the reaction on 4-hydroxy cinnamic acid with tyrosinase. Furthermore, the molecular docking was used to simulate 4-hydroxy cinnamic acid dock with tyrosinase. The results showed that 4-hydroxy cinnamic acid interacted with the enzyme active site mainly through the hydroxy competed with the substrate hydroxy group. The cytotoxicity study of 4-hydroxy cinnamic acid indicated that it had no effects on the proliferation of normal liver cells. Moreover, the results of effects of 4-hydroxy cinnamic acid on the preservation of mushroom showed that it could delay the mushroom browning. These results provide a comprehensive underlying the inhibitory mechanisms of 4-hydroxy cinnamic acid and its delaying post-harvest browning, that is beneficial for the application of this compound.
Biodegradation of ferulic acid, by an endophytic fungus Colletotrichum gloeosporioides TMTM-13 associated
with Ostrya rehderiana Chun, was explored
in this study. Ferulic acid was completely degraded by TMTM-13 as
its initial concentration was lower than 400 mg L–1. Generally, the initial concentration of ferulic acid and fungal
biomass of TMTM-13 kept synchronously growing up as the concentration
was lower than 400 mg L–1. Fungal biomass reached
a maximum of almost 1.177 g L–1 under concentrations
of 400–450 mg L–1. HPLC-MS analysis indicated
that ferulic acid ultimately degraded to vanillin, vanillic acid,
acetovanillone, and dihydroconiferyl alcohol by TMTM-13. This study
was the first report about an endophytic fungus associated with O. rehderiana Chun that has great potential for practical
application in ferulic acid contaminated environments.
AimsSemaphorin7A (Sema7A) plays an important role in the immunoregulation of the brain. In our study, we aimed to investigate the expression patterns of Sema7A in epilepsy and further explore the roles of Sema7A in the regulation of seizure activity and the inflammatory response in PTZ‐kindled epileptic rats.MethodsFirst, we measured the Sema7A expression levels in patients with temporal lobe epilepsy (TLE) and in rats of a PTZ‐kindled epilepsy rat model. Second, to explore the role of Sema7A in the regulation of seizure activity, we conducted epilepsy‐related behavioral experiments after knockdown and overexpression of Sema7A in the rat hippocampal dentate gyrus (DG). Possible Sema7A‐related brain immune regulators (eg, ERK phosphorylation, IL‐6, and TNF‐α) were also investigated. Additionally, the growth of mossy fibers was visualized by anterograde tracing using injections of biotinylated dextran amine (BDA) into the DG region.ResultsSema7A expression was markedly upregulated in the brain tissues of TLE patients and rats of the epileptic model after PTZ kindling. After knockdown of Sema7A, seizure activity was suppressed based on the latency to the first epileptic seizure, number of seizures, and duration of seizures. Conversely, overexpression of Sema7A promoted seizures. Overexpression of Sema7A increased the expression levels of the inflammatory cytokines, IL‐6 and TNF‐α, ERK phosphorylation, and growth of mossy fibers in PTZ‐kindled epileptic rats.ConclusionSema7A is upregulated in the epileptic brain and plays a potential role in the regulation of seizure activity in PTZ‐kindled epileptic rats, which may be related to neuroinflammation. Sema7A promotes the inflammatory cytokines TNF‐α and IL‐6 as well as the growth of mossy fibers through the ERK pathway, suggesting that Sema7A may promote seizures by increasing neuroinflammation and activating pathological neural circuits. Sema7A plays a critical role in epilepsy and could be a potential therapeutic target for this neurological disorder.
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