Displaying publications 1 - 20 of 1068 in total

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  1. Malays Orthop J, 2021 Mar;15(1):156.
    PMID: 33880167
    [This corrects the article DOI: 10.5704/MOJ.2011.019.][This corrects the article DOI: 10.5704/MOJ.1611.015.].
    Matched MeSH terms: Apoptosis
  2. Nordin N, Khimani K, Abd Ghani MF
    Curr Drug Discov Technol, 2021;18(6):e010921191171.
    PMID: 33563198 DOI: 10.2174/1570163818666210204202426
    BACKGROUND: Anti-apoptotic protein BCL-XL plays a vital role in tumorigenesis and cancer chemotherapy resistance, resulting in a good target for cancer treatment. Understanding the function of BCL-XL has driven the progression of a new class of cancer drugs that can mimic its natural inhibitors, BH3-only proteins, to trigger apoptosis. This mimicking is initiated through acetogenins due to their excellent biological properties. Acetogenins, which can be isolated from Annonaceae plants, have a unique structure along with several oxygenated functionalities.

    OBJECTIVE: Based on their biological capability, various acetogenins were studied in the present study and compared alongside ABT-737 on molecular docking.

    METHODS: The docking simulation of acetogenins was performed using AutoDock Vina software.

    RESULTS: Our findings have shown eleven acetogenins-BCL-XL protein complex, namely, muricin B (2), muricin F (4), muricin H (6), muricin I (7), xylomaticin (9), annomontacin (12), annonacin (14), squamocin (15), squamostatin A (16), bullatacin (20) and annoreticulin (21) exhibited strong binding affinities lower than - 10.4 kcalmol-1 as compared to ABT-373-BCL-XL complex. Six hydrogen bonds along with hydrophobic interaction were detected on the complex of BCL-XL with muricin B (2), muricin G (5), corossolone (11), and isoannonacin-10-one A (18).

    CONCLUSION: These findings indicated that some acetogenins could represent a new potential BCLXL inhibitor that could mimic the BH3-only protein for the induction of apoptosis in cancer chemotherapy.

    Matched MeSH terms: Apoptosis; Apoptosis Regulatory Proteins/pharmacology
  3. Anwar S, Malik JA, Ahmed S, Kameshwar VA, Alanazi J, Alamri A, et al.
    Molecules, 2022 Nov 08;27(22).
    PMID: 36431766 DOI: 10.3390/molecules27227668
    Cancer is the leading cause of death and has remained a big challenge for the scientific community. Because of the growing concerns, new therapeutic regimens are highly demanded to decrease the global burden. Despite advancements in chemotherapy, drug resistance is still a major hurdle to successful treatment. The primary challenge should be identifying and developing appropriate therapeutics for cancer patients to improve their survival. Multiple pathways are dysregulated in cancers, including disturbance in cellular metabolism, cell cycle, apoptosis, or epigenetic alterations. Over the last two decades, natural products have been a major research interest due to their therapeutic potential in various ailments. Natural compounds seem to be an alternative option for cancer management. Natural substances derived from plants and marine sources have been shown to have anti-cancer activity in preclinical settings. They might be proved as a sword to kill cancerous cells. The present review attempted to consolidate the available information on natural compounds derived from plants and marine sources and their anti-cancer potential underlying EMT mechanisms.
    Matched MeSH terms: Apoptosis
  4. Belmehdi O, Taha D, Abrini J, Ming LC, Khalid A, Abdalla AN, et al.
    Biomed Pharmacother, 2023 Sep;165:115205.
    PMID: 37499451 DOI: 10.1016/j.biopha.2023.115205
    α-Hederin is a natural bioactive molecule very abundant in aromatic and medicinal plants (AMP). It was identified, characterized, and isolated using different extraction and characterization technologies, such as HPLC, LC-MS and NMR. Biological tests have revealed that this natural molecule possesses different biological properties, particularly anticancer activity. Indeed, this activity has been investigated against several cancers (e.g., esophageal, hepatic, breast, colon, colorectal, lung, ovarian, and gastric). The underlying mechanisms are varied and include induction of apoptosis and cell cycle arrest, reduction of ATP generation, as well as inhibition of autophagy, cell proliferation, invasion, and metastasis. In fact, these anticancer mechanisms are considered the most targeted for new chemotherapeutic agents' development. In the light of all these data, α-hederin could be a very interesting candidate as an anticancer drug for chemotherapy, as well as it could be used in combination with other molecules already validated or possibly investigated as an agent sensitizing tumor cells to chemotherapeutic treatments.
    Matched MeSH terms: Apoptosis*
  5. Sothivelr V, Hasan MY, Mohd Saffian S, Zainalabidin S, Ugusman A, Mahadi MK
    J Cardiovasc Pharmacol, 2022 Sep 01;80(3):393-406.
    PMID: 35767710 DOI: 10.1097/FJC.0000000000001305
    Several types of cardiovascular cells use microRNA-21 ( miR-21 ), which has been linked to cardioprotection. In this study, we systematically reviewed the results of published papers on the therapeutic effect of miR-21 for myocardial infarction. Studies described the cardioprotective effects of miR-21 to reduce infarct size by improving angiogenesis, antiapoptotic, and anti-inflammatory mechanisms. Results suggest that cardioprotective effects of miR-21 may work synergistically to prevent the deterioration of cardiac function during postischemia. However, there are other results that indicate that miR-21 positively regulates tissue fibrosis, potentially worsening a postischemic injury. The dual functionalities of miR-21 occur through the targeting of genes and signaling pathways, such as PTEN , PDCD4 , KBTBD7 , NOS3 , STRN , and Spry-1 . This review provides insights into the future advancement of safe miR-21 -based genetic therapy in the treatment of myocardial infarction.
    Matched MeSH terms: Apoptosis; Apoptosis Regulatory Proteins/metabolism
  6. Ibrahim MY, Hashim NM, Omer FAA, Abubakar MS, Mohammed HA, Salama SM, et al.
    Int J Mol Sci, 2023 Jun 17;24(12).
    PMID: 37373429 DOI: 10.3390/ijms241210283
    In this study, the chemotherapeutic effect of α-mangostin (AM) was assessed in rats injected with LA7 cells. Rats received AM orally at 30 and 60 mg/kg twice a week for 4 weeks. Cancer biomarkers such as CEA and CA 15-3 were significantly lower in AM-treated rats. Histopathological evaluations showed that AM protects the rat mammary gland from the carcinogenic effects of LA7 cells. Interestingly, AM decreased lipid peroxidation and increased antioxidant enzymes when compared to the control. Immunohistochemistry results of the untreated rats showed abundant PCNA and fewer p53-positive cells than AM-treated rats. Using the TUNEL test, AM-treated animals had higher apoptotic cell numbers than those untreated. This report revealed that that AM lessened oxidative stress, suppressed proliferation, and minimized LA7-induced mammary carcinogenesis. Therefore, the current study suggests that AM has significant potential for breast cancer treatment.
    Matched MeSH terms: Apoptosis
  7. Jegathesan Y, Stephen PP, Sati ISEE, Narayanan P, Monif M, Kamarudin MNA
    Biomed Pharmacother, 2024 Mar;172:116277.
    PMID: 38377734 DOI: 10.1016/j.biopha.2024.116277
    Notorious for its high mortality rate, the current standard treatment for high-grade gliomas remains a challenge. This is largely due to the complex heterogeneity of the tumour coupled with dysregulated molecular mechanisms leading to the development of drug resistance. In recent years, microRNAs (miRNAs) have been considered to provide important information about the pathogenesis and prognostication of gliomas. miRNAs have been shown to play a specific role in promoting oncogenesis and regulating resistance to anti-glioma therapeutic agents through diverse cellular mechanisms. These include regulation of apoptosis, alterations in drug efflux pathways, enhanced activation of oncogenic signalling pathways, Epithelial-Mesenchymal Transition-like process (EMT-like) and a few others. With this knowledge, upregulation or inhibition of selected miRNAs can be used to directly affect drug resistance in glioma cells. Moreover, the clinical use of miRNAs in glioma management is becoming increasingly valuable. This comprehensive review delves into the role of miRNAs in drug resistance in high-grade gliomas and underscores their clinical significance. Our analysis has identified a distinct cluster of oncogenic miRNAs (miR-9, miR-21, miR-26a, miR-125b, and miR-221/222) and tumour suppressive miRNAs (miR-29, miR-23, miR-34a-5p, miR 181b-5p, miR-16-5p, and miR-20a) that consistently emerge as key players in regulating drug resistance across various studies. These miRNAs have demonstrated significant clinical relevance in the context of resistance to anti-glioma therapies. Additionally, the clinical significance of miRNA analysis is emphasised, including their potential to serve as clinical biomarkers for diagnosing, staging, evaluating prognosis, and assessing treatment response in gliomas.
    Matched MeSH terms: Apoptosis
  8. Hui San S, Ching Ngai S
    Gene, 2024 May 30;909:148293.
    PMID: 38373660 DOI: 10.1016/j.gene.2024.148293
    The major limitation of conventional chemotherapy drugs is their lack of specificity for cancer cells. As a selective apoptosis-inducing agent, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has emerged as an attractive alternative. However, most of the cancer cells are found to be either intrinsically resistant to the TRAIL protein or may develop resistance after multiple treatments, and TRAIL resistance can induce epithelial-to-mesenchymal transition (EMT) at a later stage, promoting cancer invasion and migration. Interestingly, E-cadherin loss has been linked to TRAIL resistance and initiation of EMT, making E-cadherin re-expression a potential target to overcome these obstacles. Recent research suggests that re-expressing E-cadherin may reduce TRAIL resistance by enhancing TRAIL-induced apoptosis and preventing EMT by modulating EMT signalling factors. This reversal of EMT, can also aid in improving TRAIL-induced apoptosis. Therefore, this review provides remarkable insights into the mechanisms underlying E-cadherin re-expression, clinical implications, and potentiation, as well as the research gaps of E-cadherin re-expression in the current cancer treatment.
    Matched MeSH terms: Apoptosis*; TNF-Related Apoptosis-Inducing Ligand/pharmacology
  9. Jorfi S, Ansa-Addo EA, Mariniello K, Warde P, Bin Senian AA, Stratton D, et al.
    J Gen Virol, 2023 Sep;104(9).
    PMID: 37665326 DOI: 10.1099/jgv.0.001884
    Like most non-enveloped viruses, CVB1 mainly uses cell lysis to spread. Details of a nonlytic virus transmission remain unclear. Extracellular Vesicles (EVs) transfer biomolecules between cells. We show that CVB1 entry into HeLa cells results in apoptosis and release of CVB1-induced 'medium-sized' EVs (CVB1i-mEVs). These mEVs (100-300 nm) harbour CVB1 as shown by immunoblotting with anti-CVB1-antibody; viral capsids were detected by transmission electron microscopy and RT-PCR revealed CVB1 RNA. The percentage of mEVs released from CVB1-infected HeLa cells harbouring virus was estimated from TEM at 34 %. Inhibition of CVB1i-mEV production, with calpeptin or siRNA knockdown of CAPNS1 in HeLa cells limited spread of CVB1 suggesting these vesicles disseminate CVB1 virions to new host cells by a nonlytic EV-to-cell mechanism. This was confirmed by detecting CVB1 virions inside HeLa cells after co-culture with CVB1i-mEVs; EV release may also prevent apoptosis of infected cells whilst spreading apoptosis to secondary sites of infection.
    Matched MeSH terms: Apoptosis*
  10. Shafee N, AbuBakar S
    FEBS Lett., 2002 Jul 31;524(1-3):20-4.
    PMID: 12135735
    Dengue virus type 2 (DENV-2) infection induced apoptotic cellular DNA fragmentation in Vero cells within 8 days of infection. The addition of high concentrations of extracellular Zn(2+) but not Ca(2+), Mg(2+) or Mn(2+) to the cell culture medium hastened the detection of apoptosis to within 4 h after infection. No apoptotic cellular DNA fragmentation was detected in the cell culture treated with Zn(2+) alone or infected with heat- or ultraviolet light-inactivated DENV-2 in the presence of Zn(2+). These results suggest that (i) apoptosis is induced in African green monkey kidney cells infected with live DENV-2 and (ii) the addition of high extracellular Zn(2+) accelerates detection of apoptosis in the DENV-2-infected cells.
    Matched MeSH terms: Apoptosis/drug effects*; Apoptosis/physiology*
  11. Harith HH, Morris MJ, Kavurma MM
    Trends Endocrinol. Metab., 2013 Nov;24(11):578-87.
    PMID: 23948591 DOI: 10.1016/j.tem.2013.07.001
    Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been extensively studied for its preferential ability to induce apoptosis of cancer cells. Beyond the cytotoxic capacity of TRAIL, new physiological and pathological roles for TRAIL have been identified, and there is now growing evidence supporting its involvement in the development of obesity and diabetes. This review summarizes the most recent findings associating TRAIL with obesity and diabetes in both humans and experimental settings. We also present and discuss some of the reported controversies behind TRAIL signaling and function. Understanding TRAIL mechanism(s) in vivo and its involvement in disease may lead to novel strategies to combat the growing pandemic of obesity and diabetes worldwide.
    Matched MeSH terms: TNF-Related Apoptosis-Inducing Ligand/metabolism*
  12. Shahdan, I.A., Rahman, M.T.
    MyJurnal
    The effectiveness of poultry stunning in producing swift slaughtering was analysed in response to the time needed for the chickens to become insensible upon neck cutting (Td) and the induction of myofiber apoptosis. In total, 49 chicken broilers (BW of 2.17 ± .24 kg) were sacrificed with pre-slaughter stunning, using a constant voltage stunner where the electric current varied between 7.2 to 124.3 mA, and without stunning. The electric current applied during stunning was found to have no effect on Td. Number of apoptotic myonuclei did not vary among stunned and unstunned meat. Apoptosis inducing factor (AIF) and caspase 3 expressions were also not detected in the meat samples of both stunned and unstunned groups at 1 d postmortem. Since the slaughtering process and stunning are associated with stress, the expression of 70 kDa-heat shock protein (Hsp70) was investigated. Moreover Hsp70 is also an inhibitor of apoptosis, by preventing the activation of AIF and apoptosome which stimulates caspase 3 activation. However, expression of Hsp70 was not induced in both stunned groups and unstunned groups. Together, this study found that poultry stunning does not affect Td and myofiber apoptosis.
    Matched MeSH terms: Apoptosis; Apoptosis Inducing Factor
  13. Abd Karim NA, Adam AHB, Jaafaru MS, Rukayadi Y, Abdull Razis AF
    Molecules, 2023 Apr 04;28(7).
    PMID: 37049977 DOI: 10.3390/molecules28073214
    Inhibition of several protein pathways involved in cancer cell regulation is a necessary key in the discovery of cancer chemotherapy. Moringa oleifera Lam is often used in traditional medicine for the treatment of various illnesses. The plant contains glucomoringin isothiocyanate (GMG-ITC) with therapeutic potential against various cancer cells. Therefore, GMG-ITC was evaluated for its cytotoxicity against the PC-3 prostate cancer cell line and its potential to induce apoptosis. GMG-ITC inhibited cell proliferation in the PC-3 cell line with IC50 value 3.5 µg/mL. Morphological changes as a result of GMG-ITC-induced apoptosis showed chromatin condensation, nuclear fragmentation, and membrane blebbing. Additionally, Annexin V assay showed proportion of cells in early and late apoptosis upon exposure to GMG-ITC in a time-dependent manner. Moreover, GMG-ITC induced a time-dependent G2/M phase arrest, with reduction of 39.1% in the PC-3 cell line. GMG-ITC also activates apoptotic genes including caspase, tumor suppressor gene (p53), Akt/MAPK, and Bax of the proapoptotic Bcl family. Early apoptosis proteins (JNK, Bad, Bcl2, and p53) were significantly upregulated upon GMG-ITC treatment. It is concluded that apoptosis induction was observed in PC-3 cells treated with GMG-ITC. These phenomena suggest that GMG-ITC from M. oleifera seeds could be useful as a future cytotoxic agent against prostate cancer.
    Matched MeSH terms: Apoptosis/genetics
  14. Yang B, Wang Q, Li Y, Li L, Zhang Y, Leong Bin Abdullah MFI, et al.
    PLoS One, 2023;18(4):e0282488.
    PMID: 37099528 DOI: 10.1371/journal.pone.0282488
    OBJECTIVE: The present study opted for the adrenal phaeochromocytoma (PC12) cell line to frame a neuronal injury model induced by alcohol exposure in vitro, aiming to probe whether TAp73 and miR-96-5p are involved in the neuronal injury process induced by alcohol and elucidate the regulatory relationship between miR-96-5p and TAp73.

    METHODS: Immunofluorescence staining was used to observe the structural features of PC12 cells after culturing in medium with nerve growth factor (NGF). After different doses and different durations of alcohol treatment, CCK-8 assay was performed to detect the viability of PC12 cells, flow cytometry assay was carried out to detect the apoptosis rate of PC12 cells, dual-luciferase reporter assay was used to definitude the regulatory relationship between miR-96-5p and Tp73, and western blot was used to detect the protein expression of TAp73.

    RESULTS: The result of immunofluorescence staining demonstrated that PC12 cells abundantly expressed Map2, CCK-8 assay illustrated alcohol exposure significantly downregulated the cell viability of PC12 cells, Treatment with miR-96-5p inhibitor induced apoptosis and upregulated the expression of TAp73 in PC12 cells. Contrastingly, miR-96-5p mimic reversed the above effects and downregulation of TAp73 inhibited the apoptosis of PC12 cells.

    CONCLUSION: The present study demonstrated that miR-96-5p participates in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73.

    Matched MeSH terms: Apoptosis/genetics
  15. Li X, Hou Q, Yuan W, Zhan X, Yuan H
    J Orthop Surg Res, 2023 Dec 01;18(1):916.
    PMID: 38041147 DOI: 10.1186/s13018-023-04412-1
    BACKGROUND: Intervertebral disc degeneration (IDD) is the main pathogenesis of low back pain. MicroRNAs (miRNAs) have been found to exert regulatory function in IDD. This study aimed to investigate the effect and potential mechanism of miR-96-5p in IDD.

    METHODS: In vitro cell model of IDD was established by treating human nucleus pulposus cells (HNPCs) with interleukin-1β (IL-1β). The level of peroxisome proliferator-activated receptor γ (PPARγ) was examined in the IDD cell model by Western blot and quantification real-time reverse transcription-polymerase chain reaction (qRT-PCR). The expression level of miR-96-5p was detected by RT-qPCR. Effects of PPARγ or/and PPARγ agonist on inflammatory factors, extracellular matrix (ECM), apoptosis, and nuclear factor-kappaB (NF-κB) nuclear translocation were examined through enzyme-linked immunosorbent assay (ELISA), Western blot, flow cytometry assay, and immunofluorescence staining. The Starbase database and dual luciferase reporter assay were used to predict and validate the targeting relationship between miR-96-5p and PPARγ, and rescue assay was performed to gain insight into the role of miR-96-5p on IDD through PPARγ/NF-κB signaling.

    RESULTS: PPARγ expression reduced with concentration and time under IL-1β stimulation, while miR-96-5p expression showed the reverse trend (P 

    Matched MeSH terms: Apoptosis/genetics
  16. Durani LW, Jaafar F, Tan JK, Tajul Arifin K, Mohd Yusof YA, Wan Ngah WZ, et al.
    Clin Ter, 2016;166(6):e365-73.
    PMID: 26794818 DOI: 10.7417/T.2015.1902
    Tocotrienols have been known for their antioxidant properties besides their roles in cellular signalling, gene expression, immune response and apoptosis. This study aimed to determine the molecular mechanism of tocotrienol-rich fraction (TRF) in preventing cellular senescence of human diploid fibroblasts (HDFs) by targeting the genes in senescence-associated signalling pathways.
    Matched MeSH terms: Apoptosis
  17. Break MKB, Chiang M, Wiart C, Chin CF, Khoo ASB, Khoo TJ
    Nutr Cancer, 2021;73(3):473-483.
    PMID: 32270712 DOI: 10.1080/01635581.2020.1751217
    Boesenbergia rotunda (L.) Mansf. is an edible herb that is commonly used in the cuisine of several Asian countries. Studies have shown that it possesses high bioactivity against a variety of cancer cells. In this study, we investigated the cytotoxic activity of Boesenbergia rotunda rhizomes and some of its constituents on nasopharyngeal carcinoma cells (HK1). MTT assay results showed that the methanolic and hexane extracts of Boesenbergia rotunda decreased HK1 cell viability with IC50 values of 136 µg/ml and 66 µg/ml, respectively. Cardamonin, a constituent of Boesenbergia rotunda, exhibited the highest cytotoxic activity with an IC50 value of 27 μg/ml. Further studies on cardamonin revealed that it inhibited the migration of HK1 cells, caused G2/M-phase arrest and induced apoptosis. Apoptosis was induced via activating caspase-8 and caspase-3, but independent of caspase-9. This indicated that cardamonin induced extrinsic apoptosis. Western blot analysis further showed that cardamonin caused extrinsic apoptosis, as the expression levels of intrinsic apoptosis-related proteins (Bcl-XL, Bcl-2 and Bax), were not affected. Finally, JC-1 staining of HK1 cells revealed an increase in the mitochondrial membrane potential after treatment, further proving that cardamonin did not induce apoptosis via the intrinsic pathway. These results reflect cardamonin's potential as an anticancer agent.
    Matched MeSH terms: Apoptosis
  18. Ngai SC
    Curr Drug Targets, 2020;21(9):849-854.
    PMID: 32116190 DOI: 10.2174/1389450121666200302124426
    Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a natural protein expressed in a wide range of tissues in our body. It is a promising anti-cancer agent due to its selective killing of cancer cells, rendering normal cells unharmed. However, resistance occurs either intrinsically or develops over the course of TRAIL treatment. In view of its specificity to cancer cells, there is a pushing need to overcome TRAIL resistance. Curcumin (Cur), a natural active constituent of turmeric, has been evidenced to have anti-cancer properties. However, it is limited by its sparing solubility and low bioavailability. Combinational therapy is one of the most frequently used strategies to overcome these limitations, which has been proved to be more effective than monotherapy by achieving synergistic effects and reducing toxicity. This review aims to discuss TRAIL and its underlying apoptotic mechanisms, the combinational treatment of Cur and TRAIL in view of their respective limitations, and the underlying apoptotic mechanisms activated by the sensitization of cancers by Cur towards TRAIL-induced apoptosis. Finally, this review discusses the research gap and the author's insight into this research area in bridging the research gap from bench to bedside.
    Matched MeSH terms: Apoptosis/drug effects*; TNF-Related Apoptosis-Inducing Ligand/pharmacology*
  19. Azman KF, Safdar A, Zakaria R
    Exp Gerontol, 2021 07 15;150:111372.
    PMID: 33905879 DOI: 10.1016/j.exger.2021.111372
    Aging is associated with a variety of morphological and functional changes in the liver. Oxidative stress and inflammation are now widely accepted as the main mechanisms involved in the aging process that may subsequently cause severe injury to mitochondrial DNA which leads to apoptosis. As aging may increase the risks for various liver diseases and plays as an adverse prognostic factor increasing the mortality rate, knowledge regarding the mechanisms of age-related liver susceptibility and the possible therapeutic interventions is imperative. Due to cost and time constraints, a mimetic aging model is generally preferred to naturally aged animals to study the underlying mechanisms of aging liver. The use of D-galactose in aging research is dated back to 1962 and has since been used widely. This review aims to comprehensively summarize the effects of D-galactose-induced aging on the liver and the underlying mechanisms involved. Its potential therapeutic interventions are also discussed. It is hoped that this invaluable information may facilitate researchers in choosing the appropriate aging model and provide a valuable platform for testing potential therapeutic strategies for the prevention and treatment of age-related liver diseases.
    Matched MeSH terms: Apoptosis
  20. Ahmad Rohi Ghazali, Fazrina Hamzah, Wan Marahaini Wan Razali, Norizah Awang
    MyJurnal
    Alpinia conchigera (lengkuas kecil) merupakan sejenis tumbuhan herba yang sering digunakan sebagai rawatan alternatif
    dalam bidang perubatan tradisional. Kajian ini dijalankan untuk menilai kesan sitotoksik, genotoksik serta mod kematian
    sel yang disebabkan oleh ekstrak heksana A. conchigera ke atas sel hepar Chang. Asai MTT selama 24 jam telah dijalankan
    untuk mengenal pasti peratus viabiliti sel hepar Chang setelah dirawat dengan ekstrak heksana A. conchigera. Keputusan
    menunjukkan terdapat penurunan viabiliti sel secara signifi kan (p < 0.05) dengan nilai IC50 (8.6 μg/ml) berbanding kawalan
    negatif. Berdasarkan nilai IC50 ini, pewarnaan AO/PI dilakukan untuk menentukan mod kematian sel hepar Chang iaitu sama
    ada secara apoptosis atau nekrosis. Didapati bahawa terdapat perbezaan secara signifi kan (p < 0.05) bagi mod kematian
    sel hepar Chang secara apoptosis berbanding kawalan negatif. Dalam kajian ini, penentuan tahap kerosakan DNA sel
    hepar Chang turut dilakukan dengan menggunakan asai komet beralkali dengan nilai IC10 dan IC25 yang diperoleh daripada
    asai MTT (4 μg/ml dan 6 μg/ml) masing-masing. Setelah sel hepar Chang dirawat dengan ekstrak heksana A. conchigera
    selama 2 jam, didapati terdapat perbezaan secara signifi kan (p < 0.05) bagi peratus kerosakan DNA bagi kumpulan rawatan
    berbanding kawalan negatif. Kesimpulannya, ekstrak heksana A. conchigera memberi kesan sitotoksik dan genotoksik
    terhadap sel hepar Chang serta menyebabkan kematian sel secara apoptosis.
    Matched MeSH terms: Apoptosis
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