The impact of CSR and green investment on stock return of Chinese export industry

A green and sustainable business environment has gained the attention of recent researchers and policymakers due to environmental and social issues globally. Therefore, the present research investigates the impact of corporate social responsibilities (CSR), green investment, green credit, and assets return on the stock return of the Chinese export industry. This study has taken the ten top export companies from China using the database of the Shanghai stock exchange. This study collected data from financial statements and stock exchange databases from 2009 to 2020. This study has used panel data analysis techniques such as robust standard error and fixed effect model (FEM) to examine the relations among the variables. The results revealed that CSR, green investment, green credit, and return on assets have a significant and positive association with the stock return of selected industries. These results imply that CSR instigates higher financial performance in the export industry; thus, improving CSR and sustainable financing promote socio-economic and societal development

Relationship between trade enhancement, firm characteristics and CSR: key mediating role of green investment

Organisations are increasingly implementing socially responsible strategies in response to increased rivalry in trade and commercial activities. Organisations are expected to increase their profitability through corporate social responsibility (CSR). Hence, this study investigates the relationship between trade enhancement, firm characteristics, and CSR. Further, this study also explored the critical mediating role of green investment (GI). The data were collected from 456 respondents from manufacturing organisations in China through a questionnaire and analysed by partial least square structural equation modelling (PLS-SEM). PLS-SEM results revealed that trade enhancement has a significant positive effect on CSR and GI. GI also has a significant effect on CSR. In comparison, firm characteristics do not have a substantial impact on CSR and GI. However, GI significantly mediates the relationship between trade enhancement, firm characteristics, and CSR. This study provides insights to managers and stakeholders regarding GI and CSR in the Chinese manufacturing industry. Lastly, this study proposes theoretical and practical implications andoffers valuable information for practitioners and policymakers

Evidence for an Induced-Fit Process Underlying the Activation of Apoptotic BAX by an Intrinsically Disordered BimBH3 Peptide

Apoptotic BAX protein functions as a critical gateway to mitochondria-mediated apoptosis. A diversity of stimuli has been implicated in initiating BAX activation, but the triggering mechanism remains elusive. Here we study the interaction of BAX with an intrinsically disordered BH3 motif of Bim protein (BimBH3) using ESR techniques. Upon incubation with BAX, BimBH3 binds to BAX at helices 1/6 trigger site to initiate conformational changes of BAX, which in turn promotes the formation of BAX oligomers. The study strategy is twofold: while BAX oligomerization was monitored through spectral changes of spin-labeled BAX, the binding kinetics was studied by observing time-dependent changes of spin-labeled BimBH3. Meanwhile, conformational transition between the unstructured and structured BimBH3 was measured. We show that helical propensity of the BimBH3 is increased upon binding to BAX but is then reduced after being released from the activated BAX; the release is due to the BimBH3-induced conformational change of BAX that is a prerequisite for the oligomer assembling. Intermediate states are identified, offering a key snapshot of the coupled folding and binding process. Our results provide a quantitative mechanistic description of the BAX activation and reveal new insights into the mechanism underlying the interactions between BAX and BH3-mimetic peptide

Arecoline inhibits the growth of 3T3-L1 preadipocytes via AMP-activated protein kinase and reactive oxygen species pathways.

The present study was designed to investigate the pathways involved in the effect of betel nut arecoline on cell viability in 3T3-L1 preadipocytes. Arecoline, but not arecaidine or guvacine, inhibited preadipocyte viability in a concentration- and time-dependent manner. Arecoline arrested preadipocyte growth in the G2/M phase of the cell cycle; decreased the total levels of cyclin-dependent kinase 1 (CDK1), p21, and p27 proteins; increased p53 and cyclin B1 protein levels; and had no effect on CDK2 protein levels. These results suggested that arecoline selectively affected a particular CDK subfamily. Arecoline inhibited AMP-activated protein kinase (AMPK) activity; conversely, the AMPK activator, AICAR, blocked the arecoline-induced inhibition of cell viability. Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins. These AMPK- and ROS-dependent effects of arecoline on preadipocyte growth may be related to the mechanism underlying the modulatory effect of arecoline on body weight

The alkaloid-dependent effect of betel nut on the production of reactive oxygen species (ROS).

<p>(A) A dose-dependent effect of arecoline was observed after 48 h of treatment. (B) Arecoline, but not arecaidine or guvacine, induced ROS production after 24 and 48 h of 400-μM treatment. ROS production was measured by the 2’,7’-dichlorofluorescein diacetate (DCFDA) method. *, <i>p</i> < 0.05 <i>vs</i>. the control.</p

Betel nut alkaloids reduced cell viability of primary preadipocytes isolated from the epididymal adipose tissues of male mice after 48 h of treatment, and the effect of arecoline depended on AMPK and ROS pathways.

<p>Data are expressed as the mean ± SEM from triplicate determinations. +, <i>p</i> < 0.1 <i>vs</i>. control; *, <i>p</i> < 0.05 <i>vs</i>. control; #. <i>p</i> < 0.05, arecoline <i>vs</i>. arecaidine, arecoline <i>vs</i>. guvacine, arecoline <i>vs</i>. NAC + arecoline, or arecoline <i>vs</i>. AICAR + arecoline (bracket); §, <i>p</i> < 0.05, 100 μM <i>vs</i>. 400 μM.</p

Effects of betel nut arecoline, but not arecaidine or guvacine, on the different phases of the cell cycle in 3T3-L1 preadipocytes.

<p>(A) A dose-dependent effect of arecoline on the cell cycle, as examined by flow cytometry, was observed after 24 and 48 h of treatment. (B) An alkaloid-specific effect of betel nut on the cell cycle was observed after 24 and 48 h of 400-μM treatment. Data are expressed as the mean ± SEM of triplicate determinations. C, control; A, arecoline; AD, arecaidine; G, guvacine. The asterisk indicates the significance of the difference (<i>p</i> < 0.05) from the control in a given phase of the cell cycle. In some groups, standard error bars are too small to be seen.</p

Effects of betel nut alkaloids on protein amounts of the cell cycle-controlling pathway proteins, such as CDK2, CDK1, p53, p21, p27, and cyclin B1, in 3T3-L1 preadipocytes.

<p>(A) A dose-dependent effect of arecoline was observed after 24 h of treatment. (B) An alkaloid-specific effect of betel nut was observed after 24 h of 400-μM treatment. These proteins were measured by Western blot analysis and then expressed after normalization to actin. In (A), we added an additional Western blot of p21 protein to the right side to indicate its significant decrease after 24 h of 400-μM arecoline treatment when compared to the control. Data are expressed as the mean ± SEM from triplicate determinations; each determination was pooled from four 10-cm culture plates. *, <i>p</i> < 0.05 <i>vs</i>. the control.</p

Arecoline, arecaidine, and guvacine differentially affected cell number and total triglyceride accumulation during the 12-day period of adipogenic differentiation of 3T3-L1 adipocytes.

<p>Data are expressed as the mean ± SEM from triplicate determinations. *, <i>p</i> < 0.05, Day 8 vs. Day 0 with no alkaloid treatment, or alkaloid vs control on Day 8 (bracket).</p

Arecoline inhibits the growth of 3T3-L1 preadipocytes via AMP-activated protein kinase and reactive oxygen species pathways - Fig 6

<p><b><i>N</i>-acetylcysteine (NAC) blocked arecoline-altered cell viability (A), reactive oxygen species (ROS) production (B), and the four different phases of the cell cycle (C) in 3T3-L1 preadipocytes.</b> 3T3-L1 preadipocytes were pretreated with NAC for 1 h and then exposed to betel nut alkaloid. After 24 and 48 h of treatment, cell viability, ROS production, and phases of the cell cycle were examined by the MTT, 2’,7’-dichlorofluorescein diacetate incorporation, and flow cytometry, respectively. In A, the NAC dosages were 0, 1.25, 2.5 and 5 mM for open circle, open square, open triangle, and closed circle, respectively, while in B and C, 5 mM NAC was used. Data are expressed as the mean ± SEM from triplicate determinations. In (A), statistical significances are not shown for clarity. *, <i>p</i> < 0.05 <i>vs</i>. the control; #, <i>p</i> < 0.05 arecoline <i>vs</i>. NAC + arecoline.</p