Nitrogen enrichment delays the drought threshold responses of leaf photosynthesis in alpine grassland plants.

Extreme drought is found to cause a threshold response in photosynthesis in ecosystem level. However, the mechanisms behind this phenomenon are not well understood, highlighting the importance of revealing the drought thresholds for multiple leaf-level photosynthetic processes. Thus, we conducted a long-term experiment involving precipitation reduction and nitrogen (N) addition. Moreover, an extreme drought event occurred within the experimental period. We found the presence of drought thresholds for multiple leaf-level photosynthetic processes, with the leaf light-saturated carbon assimilation rate (Asat) displaying the highest threshold (10.76 v/v%) and the maximum rate of carboxylation by Rubisco (Vcmax) showing the lowest threshold (5.38 v/v%). Beyond the drought thresholds, the sensitivities of leaf-level photosynthetic processes to soil water content could be greater. Moreover, N addition lowered the drought thresholds of Asat and stomatal conductance (gs), but had no effect on that of Vcmax. Among species, plants with higher leaf K concentration traits had a lower drought threshold of Asat. Overall, this study highlights that leaf photosynthesis may be suppressed abruptly as soil water content surpasses the drought threshold. However, N enrichment helps to improve the resistance via delaying drought threshold response. These new findings have important implications for understanding the nonlinearity of ecosystem productivity response and early warning management in the scenario of combined extreme drought events and continuous N deposition.

Rosmarinic Acid Protects Mice from Concanavalin A-Induced Hepatic Injury through AMPK Signaling.

Rosmarinic acid (RA) is extensively utilized in herbal medicine in China. The AMP-activated protein kinase (AMPK) signaling can be activated by RA and inhibited by the synthetic, reversible AMP-competitive inhibitor, Compound C (CC). The objective of this study was to investigate the role of AMPK signaling involving the protective effects of RA on concanavalin A (Con A)-induced autoimmune hepatitis (AIH) in mice. BALB/c mice were treated with RA, with or without CC, followed by the pretreatment with Con A. Analysis of serum aminotransferases and cytokines were conducted and liver tissue histology was performed to evaluate hepatic injury. Cytokine levels in serum and hepatic tissue were respectively measured by enzyme-linked immunoassay (ELISA) and used quantitative (q)PCR. Levels of phosphorylated acetyl CoA carboxylase in the liver, representing AMPK activation, were detected by Western blotting. Compared with the Con A group, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in RA group (100 and 150 mg/kg/d) were significantly reduced. RA also reduced hepatocyte swelling, cell death, and infiltration of leukocytes in the liver of Con A-treated mice. Serum levels of cytokines, such as interferon-γ (IFN-γ), interleukin-2 (IL-2) and interleukin-1ß (IL-1ß), were reduced by RA pretreatment, while the levels of serum interleukin-10 (IL-10), an anti-inflammatory cytokine, was elevated. These protective effects were reversed by treatment with CC. RA treatment reduced the hepatic damage via the activation of AMPK in the mice of Con A-induced. So RA acts as a potential part in the therapy of autoimmune hepatitis.

Effects of raloxifene, one of the selective estrogen receptor modulators, on pituitary-ovary axis and prolactin in postmenopausal women.

To investigate the clinical effects of raloxifene, one of the selective estrogen receptor modulators (SERMs), on the pituitary-ovary axis and prolactin, a prospective, randomized, double-blinded study on 59 healthy postmenopausal women was performed. Forty-eight women received raloxifene 60 mg daily. The other 11 received combined conjugated equine estrogen 0.625 mg and medroxyprogesterone acetate 5 mg daily (CCEP) as active controls. Serum follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and pro-lactin were measured at baseline and 1 yr after treatment. The mean levels of FSH and LH were significantly decreased in the raloxifene group (FSH: -10.7%; p < 0.01, LH: -10.3%; p < 0.05) and CCEP group (FSH: -53.7%, p < 0.001; LH: -46.8%, p < 0.001). The prolactin level decreased in the raloxifene group but not in the CCEP group (-17.0%; p < 0.001 vs +13.3%, p = no significance; NS). Consequently, long-term administration of raloxifene up to 1 yr decreases serum prolactin level significantly and may be a therapeutic alternative for postmenopausal osteoporotic women with hyperprolactinemia.