Levulinic acid (LA) is a versatile
platform chemical in the modern
concept of the biorefinery and can be used to synthesize a broad range
of desirable chemicals and fuel additives. Unfortunately, because
LA released from biomass hydrolysate is accompanied by formic acid
(FA) and 5-hydroxymethylfurfural (5-HMF), it is also important to
investigate the binary and ternary adsorption equilibrium, as well
as competitive dynamic fixed-bed column adsorption from the viewpoint
of industrial application. Batch adsorption experiments showed that
the affinity of SY-01 resin toward FA–LA–5-HMF were
in the order of 5-HMF > LA > FA under noncompetitive and competitive
systems. The highest adsorption capacity were 7.54 mg/g wet resin
for FA, 103.51 mg/g wet resin for LA, and 107.73 mg/g wet resin for
5-HMF. Interestingly, the presence of FA has a synergistic effect
on the adsorption of LA and 5-HMF onto SY-01 resin in a binary- or
ternary-mixtures system, leading to a slight increase in adsorption
uptakes. Furthermore, a mathematical model based on the general rate
model coupled with the noncompetitive single-component and competitive
multicomponent Langmuir isotherm was successfully developed to simulate
the breakthrough curves of FA–LA–5-HMF from single,
binary, as well as ternary-component mixtures. The proposed methodology
for fixed-bed column multicomponent competitive adsorption model can
be successfully implemented to completely design the separation unit
of LA from aqueous solution or biomass hydrolysate. Furthermore, it
also has the potential to expand the application to the actual biomass
hydrolysate, saving a lot of manpower and material resources.
Abstract. The hypoxia-induced proliferation of pulmonary artery smooth muscle cells (PASMCs) is the main cause of pulmonary arterial hypertension (PAH), in which oxidative stress, cyclooxygenase (COX)-2 and hydrogen sulfide (H 2 S) all play an important role. In the present study, we aimed to examine the effects of H 2 S on the hypoxia-induced proliferation of human PASMCs (HPASMCs) and to elucidate the underlying mechanisms. The HPASMCs were treated with cobalt chloride (CoCl 2 ), a hypoxia-mimicking agent, to establish a cellular model of hypoxic PAH. Prior to treatment with CoCl 2 , the cells were pre-conditioned with sodium hydrosulfide (NaHS), a donor of H 2 S. Cell proliferation, reactive oxygen species (ROS) production, COX-2 expression, prostacyclin (also known as prostaglandin I2 or PGI 2 ) secretion and H 2 S levels were detected in the cells. The exposure of the HPASMCs to CoCl 2 markedly increased cell proliferation, accompanied by a decrease in COX-2 expression, PGI 2 secretion and H 2 S levels; however, the levels of ROS were not altered. Although the exogenous ROS donor, H 2 O 2 , triggered similar degrees of proliferation to CoCl 2 , the ROS scavenger, N-acetyl-L-cysteine (NAC), markedly abolished the H 2 O 2 -induced cell proliferation, as opposed to the CoCl 2 -induced proliferation. The CoCl 2 -induced proliferation of HPASMCs was suppressed by exogenously applied PGI 2 . The addition of H 2 S (NaHS) attenuated the CoCl 2 -induced cell proliferation through the increase in the intercellular content of H 2 S. Importantly, the exposure of the cells to H 2 S suppressed the CoCl 2 -induced downregulation in COX-2 expression and PGI 2 secretion from the HPASMCs. In conclusion, the results from the current study suggest that H 2 S inhibits hypoxia-induced cell proliferation through the upregulation of COX-2/PGI 2 , as opposed to ROS.
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