The aim of this study was to investigate the contribution of lung zinc ions to pathogenesis of lung ischemia/reperfusion (I/R) injury in rats. Male Sprague Dawley (SD) rats were randomly divided into control group, lung I/R group (I/R group), lung I/R + low-dose zinc chloride group (LZnCl₂+I/R group), lung I/R + high-dose ZnCl₂ group (HZnCl₂+I/R group), lung I/R + medium-dose ZnCl₂ group (MZnCl₂+I/R group) and TPEN+MZnCl₂+I/R group (n = 8 in each group). Inductively coupled plasma mass spectrometry (ICP-MS) was used to measure the concentration of zinc ions in lung tissue. The degree of lung tissue injury was analyzed by observing HE staining, alveolar damage index, lung wet/dry weight ratio and lung tissue gross changes. TUNEL staining was used to detect cellular apoptosis in lung tissue. Western blot and RT-qPCR were used to determine the protein expression levels of caspase-3 and ZIP8, as well as the mRNA expression levels of zinc transporters (ZIP, ZNT) in lung tissue. The mitochondrial membrane potential (MMP) of lung tissue was detected by JC-1 MMP detection kit. The results showed that, compared with the control group, the lung tissue damage, lung wet/dry weight ratio and alveolar damage index were significantly increased in the I/R group. And in the lung tissue, the concentration of Zn²⁺ was markedly decreased, while the cleaved caspase-3/caspase-3 ratio and apoptotic levels were significantly increased. The expression levels of ZIP8 mRNA and protein were down-regulated significantly, while the mRNA expression of other zinc transporters remained unchanged. There was also a significant decrease in MMP. Compared with the I/R group, both MZnCl₂+I/R group and HZnCl₂+I/R group exhibited significantly reduced lung tissue injury, lung wet/dry weight ratio and alveolar damage index, increased Zn²⁺ concentration, decreased ratio of cleaved caspase-3/caspase-3 and apoptosis, and up-regulated expression levels of ZIP8 mRNA and protein. In addition, the MMP was significantly increased in the lung tissue. Zn²⁺ chelating agent TPEN reversed the above-mentioned protective effects of medium-dose ZnCl₂ on the lung tissue in the I/R group. The aforementioned results suggest that exogenous administration of ZnCl₂ can improve lung I/R injury in rats.
Animals ; Reperfusion Injury/pathology* ; Male ; Rats, Sprague-Dawley ; Rats ; Chlorides/administration & dosage* ; Lung/pathology* ; Zinc Compounds/administration & dosage* ; Apoptosis/drug effects* ; Caspase 3/metabolism* ; Cation Transport Proteins/metabolism*

The chemical constituents from green peel of Juglans sigillata were isolated by column chomatographies over silica gel, Sephadex LH-20, and MCI. Four diarylheptanoids were isolated and their structures were characterized as dihydropterocarine(1), 3',4″-epoxy-1-(4'-hydroxy-phenyl)-7-(3″-methoxyl-phenyl)-heptan-3α-ol(2), pterocarine(3), and 1-(4'-hydroxy-phenyl)-7-(3″-methoxy-4″-hydroxyphenyl)-heptan-3α-ol(4). Compound 1 is a new compound, named as dihydropterocarine. Compounds 2-4 were isolated from the plant of J. sigillata for the first time.

Objective: To investigate the chemical constituents in the shells of Juglans sigillata. Methods: The chemical constituents were isolated by silica gel, RP18, Sephadex LH-20, and MCI column chromatography and semi-preparative HPLC and so on. The structures were identified on the basis of spectroscopic analysis and chemical evidence. Results: Fifteen compounds were isolated and identified in the 70% ethanol extract from the shells of J. sigillata including seven phenolic glycosides: tachioside (1), mudanoside A (2), 4-O-β-D-glucopyranosylvanillc acid (3), breynioside A (4), 1-O-vanilloyl-β-D-glucose (5), 6'-O-vanilloyltachioside (6), and 6'-O-vanilloylisotachioside (7); three phenylpropanoide acid glycosides: 6-O-feruloyl-D-glucopyranose (8), methyl-4-O-coumaroylquinate (9), and 5-p-cis-coumaroylquinic acid (10); two tetralone glycosides: juglanin A (11) and juglanin E (12); one norsesquiterpenes glycoside: roseoside (13); one flavone: toxifolin (14); and one glucosylated abscisic acid derivate: (1'R, 3'R, 5'R, 8'S)-epi-dihydrophaseic acid β-D-glucoside (15). Conclusion: Except compound 14, the other compounds are isolated from the shells of J. sigillata for the first time. And compounds 1-4, 13, and 15 are reported for the first time from the plants in genus of Juglans L.

OBJECTIVETo investigate the inhibitory effect of polypeptide K237 on the proliferation of human hormone refractory prostate cancer cell line PC-3M and its possible mechanism.

METHODSPC-3M cells were divided into three experimental groups and a control, treated with polypeptide K237 at the concentration of 50, 100, 200 and 0 micromol/L, respectively, for 48 hours. The effects of K237 on the proliferation of different groups of the PC-3M cells were analyzed by MTF, and the mRNA expression levels of bax and bcl-2 were detected by RT-PCR.

RESULTSAfter polypeptide K237 treatment, the PC-3M cells became round, small and less transparent in cytoplasm, and some shed and suspended in the culture medium. The growth inhibition rates of the PC-3M cells were (12.6 +/- 0.95)%, (17.8 +/- 0.99)% and (27.2 +/- 1.12)% in the 50, 100 and 200 micromol/L concentration groups. RT-PCR analysis showed that the bax/beta-actin values of the 50, 100, 200 and 0 micromol/L groups were 0.919 +/- 0.071, 0.971 +/- 0.083, 0.992 +/- 0.102 and 0.889 +/- 0.067, and the bcl-2/beta-actin values of the four groups were 0.896 +/- 0.085, 0.791 +/- 0.084, 0.764 +/- 0.702 and 0.922 +/- 0.097, respectively, both with significant differences between the experimental and the control groups (P < 0.01). The mRNA expression of bax was upregulated and that of bcl-2 downregulated in a dose-dependent manner.

CONCLUSIONPolypeptide K237 may induce apoptosis of PC-3M cells by affecting the expressions of bax and bcl-2, and thus suppress the proliferation of prostate cancer cells.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Male ; Peptides ; pharmacology ; Prostatic Neoplasms ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; RNA, Messenger ; genetics ; bcl-2-Associated X Protein ; genetics ; metabolism