Aim and objectives: Natural products and derivatives of medicinal vegetation can play an important role to the cure tumor. The Present study was focused to determine the effect of Cornus mass L. extract on the induction of apoptosis in AGS gastric carcinoma cell line in compared to L929 cells. Methods: In this experimental study, AGS and L929 cells were cultured and treated with different concentrations (0-10 mg/ml) of Cornus mass L. extract for 48 and 72 hours. Cell proliferation was assessed by MTT assay. The optical density of the colored solution was quantified at 570 nm wavelengths by an ELISA Reader. Making use of the apoptosis detection kit of Annexin V-FITC, PI and double staining with Annexin V-FITC were carried out for flow cytometry investigations. Data were analyzed by ANOVA. Variations with a P-value less than 0.05 were considered significant. Results: shows a noticeable deviation among various concentrations of extract when cells were treated for 48, 72 h declined cell viability in AGS cell line in comparison L929 cell lines in a dose and time-dependent manner (P < 0.05). This extract also displayed approximately several-fold increased anti-cancer potency in AGS compared to L929 cells. The IC 50 value in AGS cells (evaluated after 48,72h) of the extract against AGS cells was 5/44, 2/44 mg/ml (p≤0.05). The analysis results of flow cytometry indicated that apoptosis was induced by the extract in AGS cells treated, compared with L929 cells. Conclusion: Each of our results implicates the reality that Cornus mass L. extract acts as a novel, potent inhibitor of cancer proliferation in in vitro. This may result in developing a promising therapeutic agent for the treatment of indole-sensitive cancers.

Adipose derived mesenchymal stem cells (ASCs) transplantation is a novel immunomodulatory therapeutic tool to ameliorate the symptom of inflammatory bowel disease (IBD). The objective of this study was to investigate the therapeutic effects of combined sufasalazine and ASCs therapy in a rat model of IBD. After induction of colitis in rats, ASCs were cultured and intraperitoneally injected (3 × 106cells/kg) into the rats on Days 1 and 5 after inducing colitis, in conjunction with daily oral administration of low dose of sulfasalazine (30 mg/kg). The regenerative effects of combination of ASCs and sulfasalazine on ulcerative colitis were assessed by measuring body weight, colonic weight/length ratio, disease activity index, macroscopic scores, histopathological examinations, cytokine, and inflammation markers profiles. In addition, western blot analysis was used to assess the levels of nuclear factor‐kappa B (NF‐κB) and apoptosis related proteins in colitis tissues. Simultaneous treatment with ASCs and sulfasalazine was associated with significant amelioration of disease activity index, macroscopic and microscopic colitis scores, as well as inhibition of the proinflammatory cytokines in trinitrobenzene sulfonic acid (TNBS)‐induced colitis. Moreover, combined ASCs and sulfasalazine therapy effectively inhibited the NF‐κB signaling pathway, reduced the expression of Bax and prevented the loss of Bcl‐2 proteins in colon tissue of the rats with TNBS‐induced colitis. Furthermore, combined treatment with ASCs and sulfasalazine shifted inflammatory M1 to anti‐inflammatory M2 macrophages by decreasing the levels of MCP1, CXCL9 and increasing IL‐10, Arg‐1 levels. In conclusion, combination of ASCs with conventional IBD therapy is potentially a much more powerful strategy to slow the progression of colitis via reducing inflammatory and apoptotic markers than either therapy alone.

Length-weight relationship, growth parameters and mortality rates of Anadara granosa in the intertidal zone of Balik Pulau, Penang Island, West Coast of Malaysia were investigated based on monthly length-frequency data (December 2011 to November 2012). A total of 548 individuals ranging from 11.25 to 33.13 mm size were subjected to analysis. Logarithmic relationship between the length and weight was Log W = 2.328 Log L − 2.537 (R2 = 0.922) for combined sexes. From this equation it was clear that the exponent ‘b’ value for A. granosa showed a negative allometric growth (b < 3). A von Bertalanffy growth function with an asymptotic length (L∞) of 35.40 mm and a growth constant (K) of 1.1 year−1 was established from length frequency distributions. The t0(−0.140) was estimated by substituting the L∞and K in the Pauly's equation. The sizes attained by A. granosa were 10.13, 14.36, 17.89, 20.82, 23.56 and 25.29 mm at the end of 2, 4, 6, 8, 10 and 12 months, respectively. The estimated growth performance index (Ø) was 3.13 while the estimated lifespan of the cockles was about 2.72 years at the study area. The estimated value of total mortality based on length-converted catch curve was Z = 3.02 year−1. The natural mortality (M) and fishing mortality (F) rates were 1.84 and 0.48 year−1, respectively. The exploitation level (E) of A. granosa was 0.20, which indicated slight fishing pressure on the stock.

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Recent advances have put fundamental focus on the application of copper (II) (Cu [II]) complexes as agents for fighting against cancer. To determine whether [Cu(L)(2imi)] complex as a novel Cu complex can induce apoptosis in HepG2 as cancerous cells and L929 as normal cells via extrinsic or intrinsic apoptotic pathways, both cell lines were treated for 24 and 48 hours at IC 50 concentrations of [Cu(L)(2imi)] complex. Then, the expression of some apoptosis-related genes including p53, caspase-8, bcl-2, and bax were assayed by real-time polymerase chain reaction. The [Cu(L)(2imi)] complex seems to inhibit the expression of bcl-2 in complex-treated HepG2 cancerous cells following the 24-and 48-hour treatment. The complex upregulated the p53, bax, and caspase-8 genes, therefore treatment of HepG2 cancerous cells with [Cu(L)(2imi)] complex induces programmed cell death via the upregulation of relative bax/bcl-2 ratio. Finally, this copper complex triggered apoptosis in HepG2 cells via both intrinsic and extrinsic pathway, whereas treatment of normal L929 cells with this complex induce apoptosis only via intrinsic pathway with the upregulation of relative bax/bcl-2 ratio and does not affect the expression level of caspase-8 gene and does not trigger the extrinsic pathway. Finally, these results obtained from present study confirm the role of a novel Cu complex on the induction of apoptosis process in HepG2 and L929 cells by overexpression of bax, inhibition of bcl-2 and increase of the relative bax/bcl-2 ratio. These results support that the [Cu(L)(2imi)] complex is able to induce apoptosis in cancerous cells, therefore, it has a potential for development as a novel anticancer drug. K E Y W O R D S bax, bcl-2, caspase-8, [Cu(L)(2imi)] complex, hepatocellular carcinoma, p53