p-Hydroxybenzaldehyde

Para?hydroxybenzaldehyde against transient focal cerebral ischemia in rats via mitochondrial preservation

Gastrodia elata (GE) Blume has been widely used for thousands of years to treat various central and peripheral nervous disorders. P-hydroxybenzaldehyde (PHBA) is a chemical component of GE. However, its role and mechanism in transient focal cerebral ischemia remain unclear. The present study aimed to investigate the protective effect of PHBA on middle cerebral artery occlusion (MCAO) rats. A total of 56 Sprague-Dawley male rats were randomly divided into control, model, PHBA-high dose (PHBA-H) and PHBA-low dose (PHBA-L) groups. The MCAO injury model was replicated in all rats except for the control group. In the control group, only the right common carotid artery was isolated without embolization. After treatment with PHBA, the protective effects (neurological deficit score, cerebral index, weight and cerebral infarct) were analyzed. Western blotting was performed to estimate the protein levels of Bcl-2, Bax and Caspase-3. Apoptotic cells were detected using hematoxylin-eosin staining and TUNEL immunofluorescence assay. Mitochondrial oxidative stress indicators, including reactive oxygen species (ROS), malondialdehyde (MDA) and total superoxide dismutase (T-SOD), while dysfunction indicators, including mitochondrial permeability transition pore (MPTP), ATP and cytochrome C oxidase, were measured using commercial kits. The ultrastructure of mitochondria was observed under an electron microscope. Once the model was successful established, the rats in the MCAO group suffered neurological damage (P<0.001), increased cerebral index (P<0.001), decreased body weight (P<0.001) and had severe cerebral infarction (P<0.001). Moreover, the number of apoptotic cells and the levels of ROS (P<0.001) and MDA (P<0.05) in mitochondria and the protein levels of Bax (P<0.001) and cleaved caspase-3 (P<0.001) were increased. The activities of T-SOD (P<0.001) and cytochrome C oxidase (P<0.001) in the mitochondria, ATP content (P<0.05) and Bcl-2 protein level (P<0.001) decreased, MPTP was stimulated to open and mitochondrial structures were damaged (P<0.001). PHBA treatment resulted in a decrease of the neurological deficit score (PHBA-H 24 h, P<0.001; PHBA-H 6 h and PHBA-L 24 h, P<0.01; PHBA-L 6 h, P<0.05), apoptotic cell number (P<0.001), mitochondrial ROS (P<0.001) and MPTP opening (P<0.001), Bax (P<0.01, P<0.001) and cleaved caspase-3 protein expression (P<0.001) in rats. And the expression of Bcl-2 protein (P<0.001) was increased. In addition, the cerebral index (P<0.05), weight loss (P<0.05), infarction rate (P<0.01) and MDA content (P<0.001) were decrease in the PHBA-H group. The level of ATP (P<0.05) and cytochrome C oxidase (P<0.05) and T-SOD activity (P<0.05) of PHBA-H group rats increased, but no significant difference was observed in the PHBA-L group. Overall, PHBA had a protective effect on transient focal cerebral ischemia in normal rats, regulated the expression of Bcl-2, Bax and cleaved caspase-3 proteins and improved the oxidative stress and dysfunction of mitochondria.

[Protective effect and mechanism of p-hydroxybenzaldehyde on blood-brain barrier]

The disruption of blood-brain barrier(BBB) induced by oxidative stress is an important pathological reaction which results in secondary brain injury during the cerebral ischemia-reperfusion. This study was designed to investigate the protective effect and mechanism of p-hydroxybenzaldehyde (p-HBA) from Gastrodia elata on BBB. The BBB is mainly consisted of vascular endothelial cells and astrocytes, so brain microvascular endothelial cell line (bEnd.3) and astrocytes (Ast) in mice were used in this study to establish BBB model. H?O?-induced oxidative stress was employed to induct the BBB damage. The bEnd.3 cells or astrocytes were exposed to different concentrations of H?O? (0.125, 0.25, 0.5, 0.75 mmol·L??) for 4 h, then exposed to 0.5 mmol·L?? H?O? for different duration (1, 2, 4, 6 h) to detect the reasonable condition of oxidative injury. After intervention by different concentrations of p-HBA(12.5, 25, and 50 mg·L??), LDH leakage rate was detected for bEnd.3 and Ast cells; the expression levels of tight junction protein claudin-5 and occludin in bEnd.3 cells were determined by Western blot and immunofluorescence. Nrf2, HO-1 and NQO1 in normal bEnd.3 cells and astrocytes as well as H?O?-induced damaged in astrocytes were detected by western blot after treatment with p-HBA. The results showed that the optimal condition of H?O? induced damage in bEnd.3 cells and astrocytes was set up as exposure the cells to 0.5 mmol·L?? H?O? for 4 h. Different concentrations of p-HBA could decrease LDH leakage rate after bEnd.3 and Ast injury was induced by H?O?; increase the protein expression levels of claudin-5, occludin, Nrf2, HO-1 and NQO1; and increase the expression levels of Nrf2, HO-1 and NQO1 in normal and H?O?-induced damaged astrocytes. These findings indicate that the p-HBA has protective effect on the BBB, and the related mechanism seems to involve up-regulating tight junction protein of the bEnd.3 cells and enhancing endogenous antioxidant capacity by activating the Nrf2/ARE pathway in both of bEnd.3 cells and astrocytes.

Simultaneous removal of 2-chlorophenol, phenol, p-cresol and p-hydroxybenzaldehyde under nitrifying conditions: kinetic study

The kinetic behavior of a stable nitrifying consortium exposed to 2-chlorophenol (2-CP), phenol, p-cresol and p-hydroxybenzaldehyde (p-OHB) was evaluated in batch assays. Phenolic compounds were evaluated either individually or in mixture. In individual assays, 2-CP inhibited stronger the nitrification, diminishing the ammonium consumption efficiency (16%) and the nitrate production rate (at 91%). Nonetheless, the consumption efficiencies for all phenolics were of 100%. On the other hand, in mixture, the inhibitory effect of 2-CP diminished significantly, since ammonium consumption efficiency and nitrate production rate were improved. Consumption efficiencies for most of the phenolic compounds were high. Furthermore, the kinetic of 2-CP oxidation was 2.4-fold-faster than the individual assays. Finally, the experimental results showed the potential of nitrifying consortium for removing 2-CP, phenol, p-cresol and p-OHB. This is the first work showing the simultaneous removal of these pollutants and also this information might be useful for treating wastewaters of chemical complexity.

The hydroxylation of P-cresol and its conversion to P-hydroxybenzaldehyde in Pseudomonas putida

Evidence of a new biotransformation pathway of p-coumaric acid into p-hydroxybenzaldehyde in Pycnoporus cinnabarinus

Pycnoporus cinnabarinus MUCL39533 was shown to be able to convert p-coumaric acid into p-hydroxybenzaldehyde, a component of high organoleptic note present in natural vanilla aroma. Use of phospholipid-enriched medium led to high-density cultures of P. cinnabarinus, since dry mycelial biomass was increased three-fold as compared to glucose medium. In the presence of phospholipids, 155 mg l(-1) p-hydroxybenzaldehyde was produced as the major compound on culture day 13 with a molar yield of 26%. The degradation pathways of p-coumaric acid were investigated. Based on the different metabolites identified, an oxidative side-chain degradation pathway of p-coumaric acid conversion to p-hydroxybenzoic acid was suggested. This acid was further reduced to p-hydroxybenzaldehyde and p-hydroxybenzyl alcohol, or hydroxylated and reduced to protocatechyl derivatives. Additionally, a reductive pathway of p-coumaric acid with 3-(4-hydroxyphenyl)-propanol as the terminal product occurred.