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M H Mei

Publications and source records attributed to M H Mei.

At least 19 recordsLinked to original sources
PubMed2000

[Protective effect of hepatocyte growth factor on hepatocyte poisoning by carbon tetrachloride and related gene expression in rats].

Hepatocyte growth factor (HGF), as a pleiotropic factor, plays important roles in organ regeneration, organogenesis and morphogenesis, but few reports on protective effect of HGF on injured liver are available. The aim of this work was to investigate protective effects of recombinant human HGF (rhHGF) on intoxicated hepatocytes induced by carbon tetrachloride (CCl4). The results are as follows: (1) rhHGF (5 ng/ml) could significantly increase the viability of hepatocytes intoxicated by CCl4 (15 mmol/L), decrease the leakage of intracellular alanine transaminase (ALT) and potassium ions into the culture medium; (2) the combination of rhHGF (5 ng/ml) and epidermal growth factor (EGF) (50 ng/ml) could increase the viability further, decrease the leakage of intracellular ALT and potassium ions of hepatocytes; (3) high expression of HGF and its receptor/c-met gene in regenerating liver after partial hepatectomy and CCl4 (50%, 2.5 ml/kg bw) poisoning were examined respectively by reverse transcription-polymerase chain reaction in rats. The results showed that rhHGF could protect hepatocytes against CCl4 through preventing intracellular ALT and potassium ion leakage, thus suggesting a synergistic effect of rhHGF and EGF on cytoprotection, and high expression of HGF and its receptor/c-met mRNA in the liver treated with PH and CCl4 poisoning. The present study suggests that the expression of HGF and its receptor gene plays an important role in liver regeneration and repair.

Animals↗
PubMed1999

Protection of regenerating liver after partial hepatectomy from carbon tetrachloride hepatotoxicity in rats: role of hepatic stimulator substance.

BACKGROUND: In the present study, we examined the effect of hepatic stimulator substance (HSS) on modulating hepatotoxicity induced by carbon tetrachloride (CCl4) in the regenerating rat liver. METHODS: Hepatotoxicity was induced in vivo by administering CCl4 to rats that had undergone a 68% partial hepatectomy (PH). In vitro studies were also performed in hepatocytes isolated from PH rats. RESULTS: Hepatic stimulator substance was extracted from regenerating rat liver 96 h after PH and its activity, as determined according to the method of LaBrecque, reached its maximum 96 h after PH. At this time, the mortality induced by CCl4 was significantly decreased in PH rats compared with sham-operated rats (18 vs 59%, P < 0.01). Likewise, changes in serum alanine aminotransferase (ALT) or bilirubin induced by CCl4 were less in rats after 96 h PH. The resistance of regenerating hepatocytes to CCl4 was retained in in vitro samples. Thus, leakage of intracellular ALT or aspartate aminotransferase induced by CCl4 in hepatocytes from 96 h hepatectomised rats was less than in control hepatocytes. HSS demonstrated a protective effect on hepatocytes against CCl4 both in vivo and in vitro. In additional studies, regenerating liver showed increased mitochondrial respiratory activity and enhanced plasma membrane fluidity. The HSS was also shown to increase hepatic mitochondrial respiratory activity and enhance plasma membrane fluidity. Further, the protective effect induced by HSS was correlated with the restoration of mitochondrial respiratory activity and plasma membrane fluidity induced by CCl4. CONCLUSIONS: Regenerating rat liver exhibits resistance to CCl4-induced hepatotoxicity, and the protection afforded by the regenerating state can be attributed, at least in part, to HSS-induced increases in mitochondrial respiratory activity and plasma membrane fluidity.

Alanine Transaminase↗
PubMed1996

[Control of growth and expression of protooncogenes in regenerating liver].

There are many humoral factors involved in the control of growth in regenerating liver. The complete hepatocyte mitogens such as hepatocyte growth factor (HGF), hepatic stimulator substance (HSS) can strongly stimulate hepatocyte DNA synthesis and mitosis. The hepatocyte growth inhibitors such as transforming growth factor beta 1 (TGF beta 1), however, do not stimulate DNA synthesis, but inhibit EGF mitogenesis. In addition, the comitogens such as norepinephrine and insulin are necessary to regulate the growth of regenerating liver. It has become clear that the hepatocyte proliferation and protooncogenes are linked closely. Some protooncogenes can express specifically as markers in the different phases of the cell cycle and in hepatocytes that enter the cell cycle (G0 to G1 transit) and continue to progress.

Animals↗
PubMed1995

[Participation of dopamine on the muscarinergic inhibitory effect of substance P on gastric myoelectric activity and motility].

Our previous study showed that microinjection of substance P (SP) into caudate nucleus inhibits gastric myoelectric fast wave and gastric motility, an effect mediated by muscarinic receptor. The present investigation showed that this effects of SP could be blocked by coinjected SP antiserum or SP antagonist [Arg6, D-Trip7,9, MePhe8]-SP6-11 or D2 dopamine antagonist haloperidol. In addition, microinjection of dopamine (DA) into caudate nucleus could also inhibit gastric fast wave and motility, an effect again being blockable by coinjected DA antagonist haloperidol or atropine. Thus, it appears that the muscarinergic inhibitory effect of SP on gastric fast wave and motility is mediated by D2 dopamine receptor.

Animals↗
PubMed1994

Using bulked extremes and recessive class to map genes for photoperiod-sensitive genic male sterility in rice.

Photoperiod-sensitive genic male sterile (PS-GMS) rice has a number of desirable characteristics for hybrid rice production. In this study we made use of a published rice genetic linkage map to determine the locations of PSGMS genes and we have characterized the effects of these genes on sterility by using molecular markers. A two-step approach was designed for mapping the genes: (i) identifying possible PSGMS gene-containing chromosome regions with bulked DNA from extreme fertile and extreme sterile plants of a very large F2 population and (ii) determining the map locations of the genes in extreme sterile individuals. We show that this mapping method is much more cost effective and statistically efficient than using a random sample of an F2 population. We identified two chromosomal regions each containing a PSGMS locus, one designated pms1 on chromosome 7 and one designated pms2 on chromosome 3. The existence of these two loci was confirmed by a large sample assay and with data on rationing progenies of the F2 plants. A marker-based analysis shows that the effect of pms1 is 2-3 times larger than that of pms2 and that dominance is almost complete at both loci. Implications in the breeding of PSGMS rice lines are discussed.

Chromosome Mapping↗
PubMed1993

Hepatic stimulator substance protects against acute liver failure induced by carbon tetrachloride poisoning in mice.

Hepatic stimulator substance was extracted from the liver of weanling Sprague-Dawley rats according to the method of LaBrecque. Quang-Ming mice were injected with carbon tetrachloride to induce acute liver failure. Hepatic stimulator substance suppressed the elevation of ALT and AST induced by carbon tetrachloride in a dose-dependent manner. Hepatic histological changes indicated that hepatic stimulator substance reduced the severity of hepatic lesion induced by carbon tetrachloride and reversed carbon tetrachloride-induced reduction of hepatic mitochondrial succinic dehydrogenase activity. In attempting to elucidate the mechanism or mechanisms of this protective effect, we found that hepatic stimulator substance significantly restored the carbon tetrachloride-induced decrease of hepatocyte plasmalemma and mitochondrial and microsomal membrane fluidity. Hepatic stimulator substance also decreased the malondialdehyde content of carbon tetrachloride-intoxicated mice; restored the liver-reduced glutathione content, which was lowered by carbon tetrachloride intoxication; stimulated liver regeneration, as shown by enhanced DNA synthesis; and increased the 3H-thymidine incorporation into DNA of hepatocytes. We propose that hepatic stimulator substance protects the liver against acute liver failure induced by carbon tetrachloride poisoning, probably by an antioxidative effect on hepatocyte membrane lipid peroxidation, which was increased by free radicals produced from carbon tetrachloride. In addition, hepatic stimulator substance stimulates hepatocyte proliferation. These protective mechanisms may act in concert to protect against carbon tetrachloride injury.

Alanine Transaminase↗
PubMed1993

[A study of regenerating liver protects against carbon tetrachloride injury in rat].

In our previous study we had demonstrated that regenerating liver of rats had an ability to resist CCl4 injury. In this paper, the underlying mechanism was further investigated. Hepatic stimulator substance from regenerating liver (rHSS) at different time after partial (68%) hepatectomy was extracted and assayed for its biological activity by using 3H-thymidine. The activity is approximately seven-fold as compared with the control. Then, rHSS was given to rats to observe its effect against CCl4 injury both in vivo and in vitro. The results were as follows: rHSS decreases the mortality of CCl4 intoxicated rats and suppresses the elevation of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) induced by CCl4 in vivo. Also rHSS increases the cell viability and decreases the leakage of intracellular ALT of hepatocytes poisoning by CCl4. The above mentioned results suggest rHSS is an important mechanism for regenerating liver to protect against CCl4 poisoning.

Animals↗
PubMed1993

[Effect of human hepatic stimulator substance on intracellular calcium and potassium homeostasis in CCl4-intoxication dissociated hepatocytes].

The human hepatic stimulator substance (hHSS) was extracted from abortive fetal liver according to the method of LaBrecque. The intracellular free calciumion was measured by fluorescent probes Fura-2/AM. Rat hepatocytes were isolated from liver by the method of Seglen and intoxicated by CCl4 vapour, then the changes of [Ca2+]i, the leakage of intracellular K+, ALT and viability of hepatocytes were observed. The results were as follows: The hHSS does exist in the human fetal liver, hHSS could increase the viability of intoxicated hepatocytes, maintain the intracellular calcium homeostasis, and decrease the leakage of intracellular potassium and ALT into the culture medium. These results indicate that hHSS could protect hepatocytes against CCl4 through maintaining calcium homeostasis, preventing potassium leakage and sustaining stability of hepatocyte polasmalemma.

Alanine Transaminase↗
PubMed1992

Effects of alcohol feeding on synthesis and secretion of apolipoproteins by regenerating rat sciatic nerve.

The amounts of apolipoprotein (apo) E and A1 released into the culture medium were examined in the regenerating nerves distal to a crush site following chronic alcohol feeding. Cultured minced segments of regenerating nerves taken from rats fed an alcohol-containing liquid diet for 5 weeks released only 50% of apoE but nearly 200% of apoA1 when compared with rats pair-fed with a control diet. The extent of decrease in medium apoE corresponded to the decrease of apoE mRNA in the nerve. Thus, chronic alcohol ingestion affects apoE synthesis of regenerating nerves by changing its mRNA level. On the other hand, apoA1 mRNA remained undetectable in regenerating and intact nerves whether the rats were fed alcohol or not. Furthermore, the amount of apoA1 released by the regenerating nerve into the culture medium was not significantly larger than that present in the nerve tissue prior to incubation. Therefore, it is most likely that apoA1 released by the injured nerve originated from the bloodstream and the increase in apoA1 content seen in the crushed nerve of alcohol-fed rats is due to an enhanced permeability of the nerve-blood barrier. Since the burst of apolipoproteins in the injured nerve is likely to play a role in nerve regeneration, the perturbation of apolipoprotein contents in regenerating nerves by chronic alcohol consumption may contribute to the pathogenesis of alcoholic neuropathy.

Alcoholism↗
PubMed1992

[A study of the protective mechanism of hepatic stimulator substance against experimental acute liver failure in mice].

In our previous work we have demonstrated a protective effect of hepatic stimulator substance (HSS) on experimental hepatic injury in mice. The underlying mechanism of this effect was further investigated with the following results: (1) HSS could significantly increase the CCl4-induced decrease of membrane fluidity of hepatic plasmalemma, mitochondria and microsomes to the control level. (2) HSS could decrease the liver melondialdehyde contents of CCl4-intoxicated mice. (3) HSS could restore the liver glutathione contents lowered by CCl4-intoxication. (4) HSS stimulated regeneration of liver, enhanced DNA synthesis of hepatocytes and increased 3H-TdR incorporation into DNA. According to the results mentioned above, we proposed that HSS should have an antioxidative effect on the hepatic membrane lipid peroxidation which was increased by free radicals produced by CCl4. In addition, HSS might increase antioxidative ability of hepatocyte and stimulate the proliferation of hepatocytes. These protective mechanisms might act in a concordant manner.

Animals↗
PubMed1992

[Effect of carbon tetrachloride intoxication on leakage of intracellular potassium in regenerating rat hepatocytes in vitro].

Leakage of intracellular potassium and GPT in normal rat hepatocytes exposed to 10, 15 and 20 mmol/L of carbon tetrachloride (CCl4) in vitro was determined at 5, 10, 15 and 20 min after cell intoxication. Both of the intracellular potassium and GPT were clearly dose- and time-dependent with CCl4, but the leakage of intracellular potassium is a more sensitive index to indicate cell injury than the later. The percent change of intracellular potassium in regenerating rat hepatocytes 20 min after CCl4 (15 mmol/L) intoxication was markedly reduced than that in normal rat. This finding indicates that regenerating hepatocytes are resistant to CCl4 hepatotoxicity in vitro, and its mechanism presumably is due to a higher stability of regenerating liver cell membrane.

Alanine Transaminase↗
PubMed1991

[Protective effect of hepatic stimulator substance against experimental acute liver failure in mice].

A hepatic stimulator substance (HSS) was extracted from the liver of male weanling SD rats according to the method of LaBrecque. The mice were injected with carbon tetrachloride or D-galactosamine to induce hepatic injuries and the protective effect of HSS on thus induced hepatic damage was investigated. The results were as follows: (1) HSS could suppresses the elevation of sGPT and sGOT induced by carbon tetrachloride intoxication in a dose-dependent manner. (2) Hepatic histological findings indicated that the degree of CCl4 or D-galactosamine-induced hepatic lesions could be lessened by HSS. (3) CCl4-induced reduction of hepatic mitochondrial succinic dehydrogenase activity could be restored by HSS. (4) Insulin-glucagon enhanced the survival of D-galactosamine intoxicated mice and stimulated hepatocyte proliferation, thus showing less pronounced hepatic damage.

Activating Transcription Factor 3↗
PubMed1991

Potentiated effect of vagal stimulation and hormonal agents on pancreatic exocrine secretion in dogs.

Chronic experiments were made on eighteen dogs with Thomas pancreatic fistula and gastric fistula. Both in chronic and acute experiments the degenerated right cervical vagus nerve was stimulated by electrical shock and the endogenous secretin and CCK was released by means of duodenal acidification (D. A.). The exogenous secretin, atropine and lidocaine were infused to analyse the interrelationship of neurohormones in the pancreatic exocrine secretion. The results were as follows. In chronic experiments the pancreatic secretory latency was shorter and volume larger than that in acute experiments induced by D. A. The difference is very significant (P less than 0.001). Both vagotomy and atropine significantly inhibited pancreatic secretion induced by D. A. (P less than 0.01). Lidocaine infused into duodenum inhibited pancreatic secretion induced by D. A. as well. When vagal stimulation was combined with D. A., either simultaneously or successively, the pancreatic secretion was increased more than the additive sum obtained by separate action of vagal stimulation and D. A. or secretin. In view of the above-mentioned facts, the author suggests that vagal impulses combined with D. A. or secretin act on the pancreatic exocrine secretion, and that the interaction of nerve and hormones appear to be mutually potentiated.

Animals↗
PubMed1990

[Effects of calcium ion on contractile response of guinea-pig gallbladder muscle strip to agonists].

The effects of calcium ion on the contractile response of gallbladder muscle strip (GBMS) in guinea pigs to acetylcholine, carbachol and caerulein were investigated by method of isotonic contraction and by RIA of cGMP and cAMP in the tissue. It was shown that the contractile response of GBMS to these agonists was stronger in Krebs solution than that in the calcium-free solution. In calcium-free solution, EDTA-zero calcium solution or verapamil-Krebs solution, the contractile response of GBMD was decreased to about 30% of the control (P less than 0.01). Verapamil significantly decreased carbachol induced enhancement of cGMP and cAMP of gallbladder tissue (P less than 0.01 or 0.05). The results suggest that both extra-and intra- cellular calcium take part in the contractile response of GBMS to agonists.

Acetylcholine↗