Today, pharmacognosy is considered a valuable science in the prevention and treatment of diseases. Among herbals, Berberine is an isoquinoline alkaloid found in the Berberis species. Surprisingly, it shows antimicrobial, antiviral, antidiarrheal, antipyretic, and anti‐inflammatory potential. Furthermore, it diminishes drug resistance in cancer therapy and enhances tumor suppression in part through autophagy and cell cycle arrest mechanisms. In the present review, we discuss the effect of berberine on diverse cellular pathways and describe how berberine acts as an autophagy modulator to adjust physiologic and pathologic conditions and diminishes drug resistance in cancer therapy.

: Curcumin is a naturally occurring polyphenol that is isolated from the rhizome of Curcuma longa (turmeric). This medicinal compound has different biological activities, including antioxidant, antibacterial, antineoplastic, and anti-inflammatory. It also has therapeutic effects on neurodegenerative disorders, renal disorders, and diabetes mellitus. Curcumin is safe and well-tolerated at high concentrations without inducing toxicity. It seems that curcumin is capable of targeting the Nrf2 signaling pathway in protecting the cells against oxidative damage. Besides, this strategy is advantageous in cancer therapy. Accumulating data demonstrates that curcumin applies four distinct ways to stimulate the Nrf2 signaling pathway, including inhibition of Keap1, affecting the upstream mediators of Nrf2, influencing the expression of Nrf2 and target genes, and finally, improving the nuclear translocation of Nrf2. In the present review, the effects of curcumin on the Nrf2 signaling pathway to exert its therapeutic and biological activities has been discussed.

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Melanoma as the most major skin malignancy has attracted much attention, so far. Although a successful therapeutic strategy requires an accurate understanding of the precise mechanisms for the initiation and progression of the melanoma. Several types of cell death mechanisms have recently been identified along with conventional cell death mechanisms such as apoptosis and necrosis. Among those mechanisms, necroptosis, anoikis, ferroptosis, and autophagy may be considered to have remarkable modulatory impacts on melanoma. In the present review, we explain the mechanisms of cell death signaling pathways related to autophagy, ferroptosis, anoikis, necroptosis, and reticulum endoplasmic stress in cells and describe how those mechanisms transduce signals in melanoma cells. Meanwhile, we describe how we can modulate those mechanisms to eliminate melanoma.

Nuclear factor erythroid 2‐related factor 2 (Nrf2) is considered as the sensor of oxidative stress, and the main aim of this signaling pathway is to maintain physiological condition by induction of redox balance. Also, this pathway exerts anti‐inflammatory effects via antioxidant response element. Oxidative stress is a key factor in a variety of pathological conditions and high level of oxidative stress is associated with damages in lipids, proteins, genetic material, and cell membrane. Multiple drugs have been developed in order to diminish oxidative stress. However, synthetic drugs suffer from various drawbacks such as high cost and side effects. On the other hand, naturally occurring compounds are of interest due to their minimal side effects and valuable biological activities. Melatonin is a hormone of pineal gland which is found in different plants. This compound has a variety of favorable biological and therapeutic activities such as antioxidant, anti‐inflammatory, anti‐tumor, anti‐diabetic, and cardioprotection. At the present review, we demonstrate that Nrf2 signaling pathway explains some of the therapeutic and biological effects of melatonin.

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This study was carried out to assess and compare the efficacy of tacrolimus and clobetasol in the treatment of oral lichen planus (OLP). The Cochrane Central Register of Controlled Trials, PubMed, Scopus, Science Direct, Springer Journals, and Elsevier databases were searched using specific keywords relevant to the research question for articles published from 1998 to December 31, 2012. Finally, 15 articles that assessed the effects of tacrolimus, clobetasol, and pimecrolimus on improvements in OLP were reviewed. In addition, a meta-analysis of odds ratios (ORs) was carried out for data in 10 of the 15 articles. The results showed that the ORs for improvements in OLP in patients taking clobetasol or tacrolimus, compared with those taking placebo or other drugs, were 1.19 and 8.00, respectively. It appears that topical tacrolimus is an effective alternative to topical clobetasol and may be considered as a first-line therapy in the management of OLP.

Regulated cell death (RCD) guarantees to preserve organismal homeostasis. Apoptosis and autophagy are two major arms of RCD, while endoplasmic reticulum (ER) as a crucial organelle involved in proteostasis, promotes cells toward autophagy and apoptosis. Alteration in ER stress and autophagy machinery is responsible for a great number of diseases. Therefore, targeting those pathways appears to be beneficial in the treatment of relevant diseases. Meantime, among the traditional herb medicine, kaempferol as a flavonoid seems to be promising to modulate ER stress and autophagy and exhibits protective effects on malfunctioning cells. There are some reports indicating the capability of kaempferol in affecting autophagy and ER stress. In brief, kaempferol modulates autophagy in noncancerous cells to protect cells against malfunction, while it induces cell mortality derived from autophagy through the elevation of p-AMP-activated protein kinase, light chain-3-II, autophagy-related geness, and Beclin-1 in cancer cells. Noteworthy, kaempferol enhances cell survival through C/EBP homologous protein (CHOP) suppression and GRP78 increment in noncancerous cells, while it enhances cell mortality through the induction of unfolding protein response and CHOP increment in cancer cells. In this review, we discuss how kaempferol modulates autophagy and ER stress in noncancer and cancer cells to expand our knowledge of new pharmacological compounds for the treatment of associated diseases. K E Y W O R D S apoptosis, autophagy, cell death, endoplasmic reticulum stress, flavonoid, kaempferol