Autophagy-related lncRNAs and exosomal lncRNAs in colorectal cancer: focusing on lncRNA-targeted strategies.

Autophagy is a cellular process that involves the degradation and recycling of cellular components, including damaged proteins and organelles. It is an important mechanism for maintaining cellular homeostasis and has been implicated in various diseases, including cancer. Long non-coding RNAs (lncRNAs) are a class of RNA molecules that do not code for proteins but instead play regulatory roles in gene expression. Emerging evidence suggests that lncRNAs can influence autophagy and contribute to the development and progression of colorectal cancer (CRC). Several lncRNAs have been identified as key players in modulating autophagy in CRC. The dysregulation of autophagy and non-coding RNAs (ncRNAs) in CRC suggests a complex interplay between these two factors in the pathogenesis of the disease. Modulating autophagy may sensitize cancer cells to existing therapies or improve the efficacy of new treatment approaches. Additionally, targeting specific lncRNAs involved in autophagy regulation could potentially be used as a therapeutic intervention to inhibit tumor growth, metastasis, and overcome drug resistance in CRC. In this review, a thorough overview is presented, encompassing the functions and underlying mechanisms of autophagy-related lncRNAs in a range of critical areas within tumor biology. These include cell proliferation, apoptosis, migration, invasion, drug resistance, angiogenesis, and radiation resistance.

Glaucocalyxin B protects against oxygen-glucose-deprivation/reperfusion-induced neuronal injury in PC-12 cells.

Oxidative stress has been implicated in the development of cerebral ischemia/reperfusion (I/R) injury. Glaucocalyxin B (GLB), one of five ent-kauranoid diterpenoids, was reported to possess neuroprotective activity. However, the effect of GLB on oxygen-glucose-deprivation/reperfusion (OGD/R)-induced cell injury in PC-12 cells has not been explored. PC-12 cells was treated with various concentrations of GLB (0, 2.5, 5 and 10 µM), and cell viability was detected using the MTT assay. PC-12 cells were pretreated with the indicated concentration of GLB (2.5-10 µM, 2 hours pretreatment), and were maintained under OGD for 3 hours, followed by 24 hours of reoxygenation. Cell viability was assessed using the MTT assay. The levels of superoxide dismutase, malondialdehyde, and glutathione peroxidase were detected using commercially available ELISA Kits. Intracellular reactive oxygen species level was measured using the fluorescent probe 2',7'-dichlorofluorescein diacetate. The levels of Bcl-2, Bax, p-Akt, Akt, p-mTOR, mTOR were detected using Western blot. Our results revealed that GLB significantly protected PC12 cells against OGD/R-induced cell injury. In addition, GLB efficiently inhibited oxidative stress and cell apoptosis in OGD/R-stimulated PC-12 cells. Mechanistic studies revealed that pretreatment with GLB could induce the activation of Akt/mTOR signaling pathway resulting in protection of OGD-treated PC12 cells. In conclusion, our data indicate for the first time that GLB protects against OGD/R-induced neuronal injury in PC-12 cells. The mechanism of the protective effect of GLB is partially associated with activation of the Akt/mTOR signaling pathway. Thus, GLB may be a potential agent for protection against cerebral I/R injury.

[Effect of hyperforin on learning and memory abilities and Aß1₋42, ßAPP and BACE1 protein expressions in hippocampus of Alzheimer's disease model mice].

To investigate the effect of the hyperforin (HF) on learning and memory function and Aß1₋42, ßAPP and BACE1 protein expressions in hippocampus of five-month-old APP/PS1 double transgenic mice, and discuss the underlying mechanism of HF. The five-month-old APP/PS1 double transgenic mice were randomly divided into the model group, rosiglitazone group (12 mg•kg⁻¹â€¢d⁻¹) and HF high dose, middle dose and low dose groups (600, 300 and 150 mg•kg⁻¹â€¢d⁻¹) in each group; in addition, 15C57BL/6J mice with the same months and background were selected as normal group. Drugs were diluted in the same volume before using, and then administrated by ig for 7 months, 1 time a day; the mice in normal group and model group received the same volume of distilled water. The learning and memory ability was tested by Morris water maze; Aß1₋42, ßAPP and BACE1proteinexpressionlevelswere tested by immunohistochemistry and Western blot. The Morris water maze results showed that as compared with the normal group, the learning and memory ability was significantly impaired in mice of model group (P<0.01); as compared with the model group, the learning and memory ability was improved in mice of rosiglitazone group and HF high, middle and low dose groups(P<0.01 or P<0.05). Immunohistochemistry and western blot results showed thatas compared with the normal group, the Aß1₋42, ßAPP and BACE1 protein expression levels in hippocampus were significantly increased in mice of model group (P<0.01);as compared with the model group, Aß1₋42, ßAPP and BACE1 protein expression levels in hippocampus were decreased in mice of rosiglitazone group and HF high, middle and low dose groups (P<0.01 or P<0.05). HF may improve the learning and memory ability of AD model mice via inhibition of ßAPP and BACE1 protein expressions, thus reduced the generation of Aß1₋42 proteins and amyloid plaque deposits in the brain.

Effect of hip replacement surgery on clinical efficacy, VAS score and Harris hip score in patients with femoral head necrosis.

AIM: To study the effect of hip replacement surgery on the clinical treatment efficacy, VAS score and Harris hip score of patients with necrosis of the femoral head (NFH). A total of 86 patients with NFH who were treated in our hospital from January 2016 to January 2019 were selected as the research subjects, and were divided into the control group (n = 43, conventional artificial hip replacement) and the observation group (n = 43, modified version of artificial hip replacement) according to a random number table method. The treatment efficacy, pain, hip function, motor function and adverse reactions of the two groups were compared. RESULTS: The effective rate of the observation group was 93.02%, which was higher than 79.07% of the control group (P<0.05). There was no difference in VAS scores of the two groups before treatment (P>0.05); after treatment, VAS scores were reduced, and the observation group was lower than the control group (P<0.05). There was no difference in Harris hip scores between the two groups before treatment; after treatment, the Harris hip joint scores were elevated, and the observation group was higher than the control group (P<0.05). There was no difference in Fugl-Meyer motor function scores between the two groups before treatment (P>0.05); after treatment, Fugl-Meyer motor function scores increased, and the observation group was higher than the control group (P<0.05). The incidence of adverse reactions in the observation group was 6.98%, which was lower than 16.28% in the control group, and the difference was not statistically significant (P>0.05). CONCLUSION: Modified artificial hip replacement is effective in treating NFH. It can relieve pain, improve hip joint function and motor function, and has high safety and is therefore worthy of promotion.

[Preparation of sinomenine hydrochloride delayed-onset sustained-release tablets].

OBJECTIVE: To prepare sinomenine hydrochloride delayed-onset sustained-release tablets. METHOD: The tablets containing sinomenine hydrochloride were prepared by dry-compression coating technique with the ratio of HPMC in core tablet and the ratio of HPMC in coating film as the influence factors and the lag-time and release rate as the evaluation parameters. Experiments were done on the central composite design, the data were simulated by using multi-linear equation and second-order polynomial equation. The possibly optimal formulation was predicted by response surface method. The dissolution date (lag-time and release rate) of the tablets prepared under the optimum condition were compared with the predicted. The drug released mechanism of the tablet were studied by Model-fitted of drug released within 6-15 h with zero-order, Higuchi and Peppas equation, respectively. RESULT: The lag-time and release rate were simulated using second-order polynomial equation, regression coefficients of the two parameters were 0.9901 and 0.9876, respectively. Bias between the observed and predicted values of lag-time and release rate were -3.15% and -0.34%, respectively. The lag-time of the tablet prepared under the optimum condition in vitro was about 6 h, then drug released from the tablet within 6-15 h was found to conform to zero-order kinetics and was controlled by bulk erosion mechanism. CONCLUSION: Sinomenine hydrochloride delayed-onset sustained-release tablets release drug slowly after lag time. The models developed in this study are proved to be highly predictable.

[Preparation of gastric retenting and chronopharmacologic drug delivery tablets of sinomenine hydrochloride].

OBJECTIVE: To prepare the gastric retenting and chronopharmacologic drug delivery tablets containing sinomenine hydrochloride as a model drug, evaluate the effects of the coating layers formulation and technics on drug release behavior, and to elucidate the mechanism of drug release based on obtained results. METHOD: The gastric retenting and chronopharmacologic drug delivery tablets were prepared by press-coated technics. The types of disintegrants were chosen according to the expanding rate and the lag-time. The effects of formulation and technics of coating layer on the release characteristic of the drug were investigated by dissolution testing. The mechanism of drug release was proved by erosion test. RESULT: The tablets had typical chronopharmacologic drug delivery properties with a lag time followed by a rapid release phase. CMS-Na was selected as the disintegrant. The lag-time was prolonged with the increase of the ratio of HPMC/carrrageenan and the amount of matrix material in coating layer. The compressing pressure and preparation method of coat material had minor influence on the lag-time of the tablets. Coating layer erosion and tablet core swelling were involved in the mechanism of drug release. CONCLUSION: The tablets had typical chronopharmacologic drug delivery properties. A suitable lag-time can be achieved by adjusting formulation of coating layer to meet the requirement of chronotherapy.