Low-carbon governance, fiscal decentralization, and enterprise green development: Evidence from China.

Simultaneously achieving economic development and environmental protection is a shared global challenge. While the positive effect of environmental regulations on protecting the environment has been widely recognized, the attention paid to low-carbon governance and corporate green transformation remains insufficient. Based on the two-stage least square regression model (2SLS) of instrumental variables, this paper utilizes panel data from China to identify the influence mechanism of government low-carbon governance on enterprise green development. It explores the effect of low-carbon governance on enterprise green development from the perspective of fiscal decentralization. The findings show that (1) Low-carbon governance significantly promotes corporate green development, primarily through improving industrial structure and technological innovation; (2) Low-carbon governance notably promotes the green development of private enterprises but has little effect on state-owned enterprises. There are also geographical differences, and the results are better in Eastern China than in the Central and Western parts of China; (3) Fiscal decentralization at both central and local levels inhibits the effect of low-carbon governance on driving corporate green development by causing a mismatch of human resources. Therefore, to promote corporate green development, low-carbon governance must prioritize green development, actively guide industrial structural upgrading and enterprise technological innovation, implement differentiated low-carbon governance measures tailored to different ownership enterprises, and optimize the assessment indicators for fiscal decentralization. This paper helps deepen the understanding of the relationship between government low-carbon governance and enterprise green development in developing countries. It can be used as a reference for government departments to formulate relevant policies.

Macrophage migration inhibitory factor is vital for inflammatory properties and survival of peripheral blood leukocytes via enhancing mitochondrial function in Ctenopharyngodon idellus.

Macrophage migration inhibitory factor (MIF) is a pleiotropic protein implicated in a broad spectrum of inflammatory and proliferative disorders. The gene sequence of grass carp (Ctenopharyngodon idella) was identified and the expression level of it was regulated by cadmium exposure in our previous study. To further clarify the immune-regulatory activity of grass carp MIF, MIF was over-expressed and interfered in grass carp peripheral blood leukocytes via transfection of plasmids pcDNA3.1-MIF-EGFP and pLKO.1-shRNA-EGFP-puro, respectively. Subsequently, survival, phagocytic capacity, mitochondrial function and cytokine production of the transfected leukocytes were assayed. The results shown that grass carp MIF was necessary for leukocyte survival, because it enhanced leukocyte viability and inhibited cell apoptosis, while MIF interference disrupted the cell viability and induced leukocyte apoptosis. The effect might benefit from improved mitochondrial function as evidenced by increased ATP production, which was due to maintained mitochondrial trans-membrane potential. In addition, MIF is essential for neutral red uptake into leukocyte, and it provoked chemokine monocyte chemotactic protein-1 (MCP-1), pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα), interleukin 1ß (IL1ß), interleukin 6 (IL6), interleukin 8 (IL8), and suppressed anti-inflammatory cytokine interleukin 10 (IL10) production. These results indicated that grass carp MIF played a vital role in regulating inflammatory properties and survival of peripheral blood leukocytes.

Allograft inflammatory factor-1 stimulates inflammatory properties of peripheral blood leukocytes and increases cell viability via enhancing mitochondrial function in Ctenopharyngodon idellus.

Allograft inflammatory factor-1 (AIF-1) is a 17 kDa calcium-binding protein associated with numerous inflammatory diseases. The full-length cDNA of AIF-1 has been identified in grass carp, Ctenopharyngodon idellus in our previous study, and it was assumed to be a novel molecule involved in immune responses. To clarify this aspect, the level of AIF-1 expression was amplified and reduced in grass carp peripheral blood leukocytes via transfection of vector pcDNA3.1-AIF1-EGFP and pLKO.1-shRNA-EGFP-puro, respectively. Thereafter, AIF-1 stimulated cell proliferation, inhibited cell apoptosis, which might benefit from improved mitochondrial function as evidenced by increased mitochondrial membrane potential, subsequently promoted ATP production. In addition, AIF-1 induced leukocyte migration via up-regulated monocyte chemotactic protein-1(MCP-1) secretion, enhanced neutral red uptake into leukocyte, provoked pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α), interleukin 1ß (IL1ß), interleukin 6 (IL6), interleukin 8 (IL8) and suppressed anti-inflammatory cytokine interleukin 10 (IL10) production. These results indicated AIF-1 played a critical role in grass carp innate immune system.