Succinic acid is an important basic raw material and intermediate used in chemical, pharmaceutical, food and agricultural fields. Due to the dual pressure of oil crisis and environmental pollution of the chemical process, the biosynthesis of succinic acid through microbial fermentation has been given much attention. In particular, the bioconversion of succinic acid from CO2 and inexpensive biomass by Actinobacillus succinogenes can reduce production costs, mitigate dependence on petroleum for specialty chemical production and lower the atmospheric CO2 concentration, thereby alleviating environmental problems. This review summarizes the new trends in the production of succinic acid by A. succinogenes. We start by introducing the unique and promising functions of A. succinogenes as a natural succinic acid producer. We then focus on the progress, challenges and future prospects of using energy crops, lignocellulosic biomass, solid waste and waste gases to produce succinic acid. Process optimization during the utilization of cheap biomass and waste gas is also highlighted. We pay particular attention to the currently known and potential promising methods to deal with the fermentation inhibitors which affects the bio-based succinic acid production. Lastly, the breeding strategies for efficient construction of A. succinogenes strains are discussed.
Glycyrrhetinic acid (GA) is an active component of licorice root that has long been used as a herbal medicine for the treatment of peptic ulcer, hepatitis, and pulmonary and skin diseases in Asia and Europe. In this study, we analyzed the effect of GA extracted from Glycyrrhiza uralensis Fisch. on the expression of Toll-like receptors (TLRs) that play key roles in regulating the innate immune response against invading pathogens. Stimulation of Ana-1 murine macrophages with GA induced a significant dose-dependent expression of TLR-4, and its mRNA expression that increased from 3-h post-treatment was approximately fivefold over the level in the mock-treated cells. No endotoxin contamination contributed to the GA-induced TLR-4 expression, because polymyxin B treatment did not alter the upregulated expression of TLR-4 in GA-treated cells. Several molecules, such as myeloid differentiation factor 88, interferon-β, and interleukin-6, which are involved in the TLR-4 downstream signaling pathway, were upregulated significantly in response to GA stimulation. Our findings demonstrate that GA is able to induce the expression of TLR-4 and activate its downstream signaling pathway.
The aim of the present study was to investigate the role of paroxetine intervention in epilepsy, and its association with the expression of serotonin transporter (SERT) and hippocampal apoptosis. Thirty adult male Sprague Dawley rats were divided into control vehicle (n=6) and epileptic (n=24) groups. Status epilepticus (SE) was induced via systemic injection of pilocarpine, and seizure activity was monitored via video electroencephalogram. The epileptic group was then randomly divided into two groups; Four weeks following SE induction, paroxetine (5 mg/kg/day; SE + paroxetine group) or normal saline (SE group) was intraperitoneally injected for 4 weeks. Brain tissue was collected to evaluate apoptosis via terminal deoxynucleotidyl transferase dUTP nick‑end labeling. SERT, B‑cell lymphoma‑2 (Bcl‑2) and brain derived neurotropic factor (BDNF) expression levels were evaluated by western blotting, and miR‑16 expression was evaluated by reverse transcription‑quantitative polymerase chain reaction. Paroxetine did not affect the mortality of the pilocarpine‑induced chronic epileptic rats. Spontaneous recurrent seizures (SSRs) were observed 7‑28 days following SE induction. The frequency and stage of the SSRs were reduced by paroxetine administration. Apoptotic cells were observed in the epileptic hippocampus. Following paroxetine intervention, the staining intensity and number of apoptotic cells were significantly decreased. Expression levels of BDNF and Bcl‑2 were lower in the SE group compared with the vehicle group. The former was not altered by paroxetine injection; however, the latter was increased. In the SE group, SERT expression was not altered in the raphe nucleus but was decreased in the hippocampus. Following paroxetine administration, SERT expression was decreased in the raphe nucleus and increased in the hippocampus. In the SE group, miR‑16 expression was decreased in the raphe nucleus and increased in the hippocampus. Following paroxetine administration, miR‑16 expression was not altered in the raphe nucleus but was reduced in the hippocampus. In conclusion, the seizures and hippocampal apoptosis observed in chronic epileptic rats were alleviated by paroxetine treatment. This effect may be associated with the reduced Bcl‑2 and BDNF expression and the modulation of SERT expression. The alterations in miR‑16 expression may provide a potential explanation for the modulation of apoptosis; however, further research is required to determine the complete underlying molecular mechanism.
This study investigated the effects of dietary exogenous protease on the growth performance, intestinal health, immune parameters and disease resistance of genetically improved farmed tilapia (GIFT, Oreochromis niloticus). Five test diets with commercial protease at the levels of 0, 1.38, 2.76, 5.52 and 11.04 U/g (named PE0, PE1, PE2, PE5 and PE11, respectively) were administered to triplicate tanks with 30 fish for 60 days, and then, the fish were challenged with Streptococcus agalactiae for 14 days. The results indicated that weight gain increased as exogenous protease increased from 0 to 5.52 U protease/g diet and then decreased significantly (p < .05) with a further increase in exogenous protease supplementation (p < .05). The height of the villi in the proximal intestine and distal intestine, the width of the villi in three segments of the intestine, and the thickness of the muscle layer in the proximal intestine and mid-intestine (p < .05) were increased in the fish fed the PE5 diet. Immune and antioxidant indices (except malondialdehyde), and survival after challenged with S. agalactiae were higher in fish fed PE5 diets than in those fed other diets (p < .05). In conclusion, 5.52 U/g protease supplementation in a plant-based diet could promote the growth performance, intestinal physical barrier function, innate immunity and S. agalactiae resistance of GIFT.
Long noncoding RNA intersectin 1-2 (lnc-ITSN1-2) regulates inflammation and neuronal apoptosis; meanwhile, the latter two factors participate in the pathogenesis of acute ischemic stroke (AIS). Therefore, this study detected lnc-ITSN1-2 at multiple time points, aiming to explore its longitudinal variation and clinical value in the management of AIS patients.The current study enrolled 102 AIS patients, then detected their lnc-ITSN1-2 in peripheral blood mononuclear cell (PBMC) at baseline (D0), day (D)1, D3, D7, month (M)1, M3, M6, and year (Y)1 after admission using RT-qPCR. Additionally, lnc-ITSN1-2 in PBMC of 50 controls was also detected.Lnc-ITSN1-2 was up-regulated in AIS patients than that in controls (p < 0.001). Lnc-ITSN1-2 positively associated with NIHSS score, TNF-α, and IL-17A (all p < 0.050) but was not linked with IL-6 (p = 0.093) in AIS patients. Notably, lnc-ITSN1-2 was gradually increased from D0 to D3; while it switched to decrease from D3 to Y1 in AIS patients. Lnc-ITSN1-2 disclosed similar longitudinal variation during 1 year in non-recurrent (p < 0.001), recurrent (p = 0.001), and survived patients (p < 0.001), while the variation of lnc-ITSN1-2 in died patients was not obvious (p = 0.132). More importantly, lnc-ITSN1-2 at D0, D3, D7, M1, M3, M6, and Y1 was higher in recurrent AIS patients than that in non-recurrent AIS patients (all p < 0.050); moreover, lnc-ITSN1-2 at D3, D7, M1, M3, and M6 was up-regulated in died AIS patients than AIS survivors (all p < 0.050).The dynamic variation of Inc-ITSN1-2 could serve as a biomarker reflecting disease severity, inflammatory cytokines, recurrence, and death risk in AIS patients.
ACE inhibitory dipeptides from Xerocomus badius fermented shrimp processing waste were isolated with ethanol, macroporous resin, chloroform, and Sephadex G-10 in sequence and identified by LC-MS/MS system coupled with electrospray ionization source. Molecular docking was performed for exploring the mechanism of their inhibitions. The results showed that the identified ACE inhibitory dipeptides were Cys-Cys and Cys-Arg with IC 50 values of 4.37 ± 0.07 and 475.95 ± 0.11 μ M, respectively. The difference between ACE inhibitor potency of Cys-Cys and Cys-Arg could be explained by results of molecular docking. Cys-Cys formed crucial coordination between carboxyl oxygen and Zn(II), hydrogen bonds with residues Ala354(O), Ala356(HN), and Tyr523(OH), and a bump with the residue His387(NE2) at the active site of ACE. There was no coordination, except for 5 hydrogen bonds (at residues His353, Ala354, Glu384, Glu403, and Arg522) and a bump (Glu411) between Cys-Arg and active site of ACE. These findings highlighted that Cys-Cys could be considered as a novel potent ACE inhibitor, and coordination between its carboxyl oxygen and Zn(II) played significant role in defining its ACE inhibitor potency.
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